Affinage

GDF11

Growth/differentiation factor 11 · UniProt O95390

Length
407 aa
Mass
45.1 kDa
Annotated
2026-06-10
100 papers in source corpus 41 papers cited in narrative 41 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GDF11 is a secreted TGF-β superfamily ligand that signals through activin type II receptors (ActRIIA and ActRIIB) and type I receptors (ALK4/5/7) to activate canonical SMAD2/3 phosphorylation, controlling rostrocaudal axial patterning, progenitor cell-cycle exit, and adult tissue homeostasis across multiple organs (PMID:12414726, PMID:16790475, PMID:28257634). It is produced as a latent precursor activated by ordered proteolysis: proprotein convertases including PC5/6 (PCSK5) cleave the RSRR↓N motif, and BMP1/Tolloid metalloproteinases subsequently cleave the noncovalent prodomain complex to release active ligand (PMID:15988002, PMID:18378898). In developmental patterning, GDF11 signaling drives caudal Hox gene expression through direct SMAD2/3 binding to axial Hox enhancers (e.g., the Hoxd11 region VIII Smad3/4 element), positioning vertebrae, hindlimbs, and spinal motor neuron columns (PMID:16790475, PMID:24016758, PMID:29046533). As a negative-feedback regulator of neurogenesis, GDF11 induces p27Kip1 and p57Kip2 to enforce reversible cell-cycle arrest in neuronal progenitors, limiting their number in both embryonic and adult neurogenic niches; it likewise restrains pancreatic NGN3+ islet progenitor expansion while promoting beta-cell maturation (PMID:12546816, PMID:21248112, PMID:34488822, PMID:15548585). In adult tissues GDF11 acts through SMAD2/3 to repress Runx2 and osteoblast differentiation, and to induce skeletal and cardiac muscle atrophy via a SMAD2/3→FOXO1→Atrogin-1 axis engaging the ubiquitin-proteasome pathway (PMID:27395058, PMID:28270449, PMID:36094432). Extracellularly its activity is blocked by antagonists including GASP-1, GASP-2, and the WFIKKN2 follistatin domain, which prevent type II receptor binding (PMID:24019467, PMID:30814254). A loss-of-function variant at the furin cleavage site (p.Arg298Gln) causes a human syndrome of cleft lip/palate and vertebral/rib anomalies mirroring Gdf11-null mice, establishing GDF11 processing as essential for human development (PMID:31215115).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 2001 Medium

    Established GDF11 as a diffusible morphogen that negatively regulates differentiation and induces Hox gene expression, defining its role in axial and limb patterning.

    Evidence Bead implantation and micromass assays in chick wing buds with Hox and follistatin expression readouts

    PMID:11203700 PMID:11754833

    Open questions at the time
    • Receptor identity and intracellular transducer not defined in these early studies
    • Avian gain-of-function only; endogenous requirement not tested
  2. 2002 High

    Identified the receptor system, showing GDF11 binds ActRIIA and ActRIIB and induces Smad2 phosphorylation to pattern axial vertebrae, anchoring the signaling pathway in vivo.

    Evidence Double-mutant mouse genetics, biochemical receptor binding, and Smad2 phosphorylation assays

    PMID:12414726

    Open questions at the time
    • Type I receptor partner not resolved in this study
    • Direct transcriptional targets downstream of Smad2 not identified
  3. 2003 High

    Defined GDF11 as a negative-feedback regulator of neurogenesis acting through p27Kip1-mediated cell-cycle arrest, explaining how progenitor numbers are autoregulated.

    Evidence Gdf11 and follistatin knockout mice with in vitro neurogenesis and p27Kip1 expression analysis

    PMID:12546816

    Open questions at the time
    • How GDF11 levels are sensed to set the feedback threshold not defined
    • Receptor complex in olfactory progenitors not specified
  4. 2005 High

    Resolved the activation mechanism: GDF11 is held latent by its SPC-cleaved prodomain and liberated by BMP1/Tolloid cleavage, identifying a key control point on ligand bioavailability.

    Evidence In vitro reconstitution of the latent complex, cleavage-site mutagenesis, and PC12 differentiation assays

    PMID:15988002

    Open questions at the time
    • In vivo contribution of BMP1/Tolloid versus other proteases not quantified
    • Spatial regulation of activation in tissues not addressed
  5. 2005 High

    Showed GDF11 controls competence timing rather than proliferation, setting the Math5 expression window that limits retinal ganglion cell genesis — distinguishing a timing mechanism from a proliferative one.

    Evidence Gdf11 knockout mice with retinal cell counting and Math5 expression analysis

    PMID:15976303

    Open questions at the time
    • Molecular link between Smad signaling and Math5 regulation not defined
    • Mechanism distinguishing competence from proliferation control unclear
  6. 2006 High

    Established the Gdf11→Smad2→caudal Hox pathway for rostrocaudal spinal identity by gain- and loss-of-function across species, formalizing the signaling logic of axial patterning.

    Evidence In ovo electroporation, Gdf11 knockout analysis, and Smad2 phosphorylation assays

    PMID:16790475

    Open questions at the time
    • Whether Smad2 acts directly at Hox enhancers not yet shown (later addressed in 2013)
    • Cofactors conferring caudal specificity unknown
  7. 2004 High

    Placed GDF11-Smad2 signaling in pancreatic islet differentiation, showing it restrains NGN3+ progenitor number and is required for beta-cell maturation.

    Evidence Gdf11-null and Smad2-null mouse models with histological and molecular analysis of pancreas

    PMID:15548585

    Open questions at the time
    • Relationship to Notch signaling defined only as parallel, not mechanistically integrated
    • Direct transcriptional targets in islet progenitors not identified
  8. 2008 High

    Identified PC5/6 as the proprotein convertase cleaving GDF11 at RSRR↓N in vivo, defining selectivity determinants of the first activating cleavage.

    Evidence Conditional knockout, in vitro cleavage assays, and in situ hybridization

    PMID:18378898

    Open questions at the time
    • Redundancy with furin and other convertases not fully resolved
    • Tissue-specific convertase usage not mapped
  9. 2011 High

    Refined the neurogenic feedback model by distinguishing GDF11 (inhibits immediate neuronal precursors) from activin βB (inhibits stem/early progenitors) and identifying additional effectors p57Kip2 and Pax6.

    Evidence Multi-mutant mouse genetics, neurosphere assays, and Western blots for cell-cycle regulators

    PMID:21248112 PMID:21852401

    Open questions at the time
    • How distinct progenitor populations respond differentially to related ligands unclear
    • Receptor-level basis for GDF11 versus activin specificity not defined
  10. 2009 Medium

    Demonstrated GDF11 maintains hESC self-renewal through type I TGF-β receptor (ALK4/5/7)–dependent SMAD2/3 activation and revealed Foxg1 antagonizes GDF11 feedback in neurogenesis via genetic epistasis.

    Evidence hESC culture with SB431542 inhibition and compound-mutant genetic rescue in mouse olfactory epithelium

    PMID:19297409 PMID:19751112

    Open questions at the time
    • Direct Foxg1–Smad biochemical interaction not fully resolved
    • hESC pluripotency role uses pharmacology that does not isolate GDF11 from related ligands
  11. 2013 High

    Provided direct molecular evidence that Smad2/3 binds axial Hox enhancers and identified GASP-2 as an in vivo GDF11 antagonist acting by blocking type II receptor binding.

    Evidence ChIP, enhancer mutagenesis, transgenic embryos, plus receptor-binding blocking assays and Gasp1/Gasp2 knockout skeletal phenotyping

    PMID:24016758 PMID:24019467

    Open questions at the time
    • Full repertoire of direct Smad-bound Hox enhancers not mapped
    • GASP antagonist tissue specificity and relative potency versus follistatin not defined
  12. 2015 High

    Using a GDF11-specific immunoassay, showed GDF11 and myostatin share identical SMAD2/3-mediated inhibition of myoblast differentiation and that GDF11 inhibits muscle regeneration, reframing GDF11 as a potential negative regulator of muscle.

    Evidence Validated GDF11-specific immunoassay, SMAD2/3 phosphorylation, myoblast differentiation, and in vivo regeneration assays

    PMID:26001423

    Open questions at the time
    • Molecular features distinguishing GDF11 from myostatin in muscle not resolved here
    • Endogenous circulating GDF11 dynamics across age debated
  13. 2016 Medium

    Extended GDF11's catabolic role to bone, showing SMAD2/3-mediated Runx2 repression inhibits osteoblast differentiation and accelerates age-related bone loss.

    Evidence In vitro osteoblast differentiation, Runx2 analysis, and in vivo GDF11 injection with bone histomorphometry

    PMID:27395058

    Open questions at the time
    • Reconciliation with later genetic evidence of a pro-osteogenic role not addressed
    • Dose dependence of bone effects not delineated
  14. 2017 High

    Crystal structures explained GDF11's greater potency over GDF8 via type I receptor binding-site features and confirmed supraphysiological GDF11 drives skeletal and cardiac atrophy through SMAD2/3 and the ubiquitin-proteasome pathway.

    Evidence X-ray crystallography with mutagenesis and signaling assays; AAV-mediated systemic overexpression with muscle mass measurement

    PMID:28257634 PMID:28270449

    Open questions at the time
    • Physiological versus supraphysiological dose effects remain a central ambiguity
    • Cardiac specificity attributed to TGFβR1 expression not mechanistically proven
  15. 2017 High

    Defined a tumor-suppressive mechanism in which PCSK5 mobilizes a sequestered latent GDF11 reservoir to suppress breast cancer metastasis, linking convertase processing to disease.

    Evidence PCSK5 reconstitution in TNBC cells, invasion assays, intraductal xenografts, and precursor/mature GDF11 Western blots

    PMID:29161592

    Open questions at the time
    • Generality of precursor sequestration across cancer types unknown
    • Receptor and transcriptional output mediating metastasis suppression not detailed
  16. 2019 Medium

    Established a human Mendelian link: a furin-site GDF11 variant (p.Arg298Gln) impairs processing and causes craniofacial and axial skeletal anomalies, and structural work defined how WFIKKN2 antagonizes GDF11.

    Evidence Exome sequencing with functional assays and zebrafish model; WFIKKN2 follistatin-domain crystal structure with SPR and alanine scanning

    PMID:30814254 PMID:31215115

    Open questions at the time
    • Full phenotypic spectrum of GDF11 variants in humans not catalogued
    • Relative in vivo contribution of WFIKKN2 versus other antagonists unquantified
  17. 2019 Medium

    Broadened GDF11 context-dependent signaling beyond canonical SMAD2/3, documenting ALK5-dependent effects in hepatocellular carcinoma lipid handling, ERK/SMURF1-mediated hepcidin suppression, and ID2→MMP2-driven trophoblast invasion.

    Evidence ALK5 inhibitor (SB431542), transcriptomics/lipidomics, SMURF1 and ERK pathway analysis, and siRNA invasion assays across hepatocyte, hepatic, and trophoblast systems

    PMID:31418854 PMID:33684566 PMID:35705978

    Open questions at the time
    • Cell-type determinants of divergent (SMAD versus ERK/PI3K) output not defined
    • Most effects shown in single-lab cell models without genetic confirmation
  18. 2020 High

    Genetic models complicated the bone story, showing Gdf11-null mice have reduced bone mass via BMP signaling and opposing myostatin, establishing GDF11 as pro-osteogenic and revealing antagonist-dependent context.

    Evidence Gdf11-/- and Mstn-/- mouse models with bone mass measurement, differentiation assays, and BMP signaling analysis

    PMID:32071240

    Open questions at the time
    • Mechanistic reconciliation with SMAD2/3-mediated Runx2 repression in osteoblasts not achieved
    • Conditions favoring SMAD2/3 versus BMP output in bone unclear
  19. 2022 Medium

    Resolved the muscle-atrophy mechanism in human cells as a SMAD2/3→FOXO1→Atrogin-1 axis, providing a defined transcriptional route from ligand to proteolytic atrophy.

    Evidence Human iPSC-derived myocytes with FOXO1 inhibition, SMAD2/3 phosphorylation, and Atrogin-1 expression analysis

    PMID:36094432

    Open questions at the time
    • Whether this axis operates at physiological GDF11 levels in vivo not established
    • Single human cell model, no in vivo genetic confirmation
  20. 2021 High

    Inducible adult conditional knockout confirmed endogenous GDF11 remains a negative regulator of adult hippocampal neurogenesis, extending the developmental feedback role into adulthood.

    Evidence Tamoxifen-inducible Gdf11 conditional knockout with progenitor proliferation and newborn neuron quantification

    PMID:34488822

    Open questions at the time
    • Receptor and effector identity in adult niche not specified
    • Functional/behavioral consequences not assessed
  21. 2023 Medium

    Characterized GDF11's cardiac injury context, showing systemic GDF11 augments infarct size via pro-apoptotic signaling and correlates with age-associated circulating levels in human MI patients.

    Evidence Recombinant GDF11 delivery in ischemia-reperfusion mice, targeted transcriptomics, and validated LC-MS/MS GDF11 assay in patients

    PMID:37742057

    Open questions at the time
    • Direct versus indirect apoptotic mechanism not fully separated
    • Causality of human circulating GDF11 versus correlation not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single ligand produces opposite tissue outcomes (e.g., catabolic versus pro-osteogenic bone effects, beneficial versus harmful cardiac effects) and what determines the choice between SMAD2/3, SMAD1/5/8, and non-canonical (ERK/PI3K/Ca2+) outputs at physiological doses.
  • No unified model reconciling dose-, receptor-, and context-dependent signaling outputs
  • Physiological versus supraphysiological effect thresholds not defined across tissues
  • Antagonist-dependent switching of downstream pathway output not mechanistically mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 3 GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 2
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-392499 Metabolism of proteins 4 R-HSA-162582 Signal Transduction 3
Partners
ACVR1BACVR2AACVR2BBMP1FSTPCSK5TGFBR1WFIKKN2

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 Gdf11 signals through both activin type IIA (ActRIIA) and type IIB (ActRIIB) receptors to pattern axial vertebrae; biochemical studies showed Gdf11 binds both receptors and induces phosphorylation of Smad2. Genetic studies demonstrated ActRIIA and ActRIIB cooperatively mediate Gdf11 signaling, and each can compensate for the other. Genetic epistasis (double mutant mice), biochemical binding assays, Smad2 phosphorylation assays Genes & development High 12414726
2005 GDF11 forms a noncovalent latent complex with its SPC-cleaved prodomain, and this latent complex is activated by cleavage at a single specific site by BMP1/Tolloid family metalloproteinases. Mutant GDF11 prodomains resistant to BMP1/Tolloid cleavage act as potent stimulators of neural differentiation. In vitro biochemical reconstitution, mutagenesis of protease cleavage site, cell differentiation assays (PC12 cells) Molecular and cellular biology High 15988002
2008 The proprotein convertase PC5/6 (PCSK5) cleaves GDF11 at the RSRR↓N motif (P1' Asn determining selectivity) in vivo; PC5/6-deficient embryos display Gdf11-related phenotypes including altered anteroposterior patterning. In vitro and ex vivo analyses confirmed PC5/6 selectivity for GDF11. Conditional gene knockout, in vitro cleavage assays, ex vivo analysis, in situ hybridization Proceedings of the National Academy of Sciences of the United States of America High 18378898
2003 GDF11 mediates negative autoregulatory feedback inhibition of olfactory epithelium neurogenesis by inducing p27(Kip1) expression and reversible cell cycle arrest in neuronal progenitors. Mice lacking GDF11 have more progenitors and neurons; mice lacking follistatin (a GDF11 antagonist) show dramatically decreased neurogenesis. Mouse knockout, in vitro neurogenesis assays, p27Kip1 expression analysis Neuron High 12546816
2001 FGFs, Gdf11, and retinoid signals from Hensen's node and paraxial mesoderm converge to establish Hox-c positional identity of spinal motor neurons along the rostrocaudal axis of the developing spinal cord. In vitro patterning assay with chick embryos, Hox-c protein expression profiling, signal perturbation experiments Neuron Medium 11754833
2006 Ectopic Gdf11 expression in chick spinal cord causes rostral displacement of Hoxc protein expression domains and motor neuron column positions; follistatin (Gdf11 antagonist) has the converse effect. Gdf11 induces Smad2 phosphorylation, and activated Smad2 induces caudal Hox gene expression, establishing Gdf11→Smad2→Hox as the pathway for rostrocaudal identity in the spinal cord. In ovo electroporation, Gdf11 knockout mouse analysis, Smad2 phosphorylation assays Development (Cambridge, England) High 16790475
2004 GDF11 negatively regulates the number of NGN3+ islet progenitor cells in the pancreas and is required for beta-cell maturation. Mice deficient in Gdf11 have excess NGN3+ cells but reduced beta-cells. Similar phenotypes occur in mice deficient for SMAD2, placing GDF11-Smad2 signaling in the islet differentiation pathway parallel to Notch. Mouse knockout (Gdf11-null and Smad2-null), histological and molecular analysis of pancreatic development Development (Cambridge, England) High 15548585
2005 GDF11 controls the temporal window of Math5 expression in retinal progenitors, thereby determining the duration of competence for retinal ganglion cell (RGC) genesis. GDF11 acts not by affecting progenitor proliferation but by controlling the timing of Math5 expression. Mouse knockout, retinal cell counting, Math5 expression analysis Science (New York, N.Y.) High 15976303
2011 In the olfactory epithelium, GDF11 inhibits proliferation and expansion of immediate neuronal precursors (INPs), while activin βB (ACTβB) inhibits expansion of stem/early progenitor cells by a distinct mechanism. Interplay between GDF11, ACTβB, and follistatin controls both total cell number and the ratio of neuronal vs. glial cells. Mouse genetics (Fst-/- and double mutants), cell-type-specific marker analysis, in vitro neurosphere assays Development (Cambridge, England) High 21852401
2011 Gdf11 secreted by newly born neurons in the developing spinal cord facilitates temporal progression of neurogenesis by upregulating p57(Kip2) and p27(Kip1) and downregulating Pax6 in progenitors, promoting cell cycle exit and reducing proliferation potential. Gdf11-/- mouse analysis, neurosphere assays, in vitro Gdf11 addition, Western blot for cell cycle regulators The Journal of neuroscience : the official journal of the Society for Neuroscience High 21248112
2013 GASP-1 and GASP-2 inhibit GDF11 (and myostatin) activity by blocking binding of the ligand to the type II receptor. Mice lacking Gasp2 show posterior transformations of the axial skeleton (opposite to Gdf11-/- anterior transformations), confirming GASP-2 as a GDF11 inhibitor in vivo. Biochemical receptor-binding blocking assays, genetic mouse models (Gasp1-/-, Gasp2-/-), skeletal phenotype analysis, muscle fiber-type assessment Proceedings of the National Academy of Sciences of the United States of America High 24019467
2013 Gdf11/Smad signaling directly activates the Hoxd11 axial expression enhancer via a conserved Smad3/4 binding element (region VIII). Chromatin immunoprecipitation demonstrated direct Smad2/3 protein binding to the Hoxd11 enhancer; mutation of the Smad binding motif abolishes Gdf11-induced reporter activity and is essential for axial Hoxd11 expression in the embryo tailbud. Reporter assays (luciferase, lacZ), mutagenesis of Smad-binding element, ChIP, SIS3 (Smad3 inhibitor) treatment, transgenic mouse experiments Developmental biology High 24016758
2009 Foxg1 promotes olfactory neurogenesis by antagonizing Gdf11-mediated negative feedback. Foxg1 binds Smad transcriptional complexes and can bind Gdf11-related signaling; loss of one allele of Gdf11 substantially rescues neurogenesis defects in Foxg1-/- OE, demonstrating genetic epistasis. Genetic rescue experiments (Foxg1-/-;Gdf11-/- and Foxg1-/-;Gdf11+/- compound mutants), OE neurogenesis quantification, Fst expression analysis Development (Cambridge, England) High 19297409
2013 GDF11 activates the canonical Smad2/3 signaling cascade in neural stem cells (Cor-1 line) via an ActRIIB/ALK5 receptor complex, significantly alters expression of ~4700 gene transcripts, suppresses cell proliferation by downregulating Cyclin D2, and inhibits migration by reducing Fascin and LASP1 expression. Receptor identification, Smad2/3 signaling assay, transcriptomic profiling, cell proliferation and scratch-wound migration assays, siRNA knockdown of EGF receptor PloS one Medium 24244313
2017 Crystal structures of apo-GDF11, apo-GDF8, and the GDF11:FS288 complex revealed unique structural features in the type I receptor binding site of GDF11 that confer greater potency. GDF11 is a more potent activator of SMAD2/3 and signals more effectively through ALK4/5/7 than GDF8; substitution of GDF11 residues into GDF8 enhances GDF8 activity. X-ray crystallography, SMAD2/3 phosphorylation assays, mutagenesis (GDF11 residue substitution into GDF8), receptor binding assays BMC biology High 28257634
2015 GDF11 and myostatin both induce SMAD2/3 phosphorylation and inhibit myoblast differentiation, regulating identical downstream signaling. Using a GDF11-specific immunoassay (GDF11-specific reagents), GDF11 levels show a trend toward increase rather than decrease in aged rats and humans, and GDF11 significantly inhibited muscle regeneration and decreased satellite cell expansion in mice. GDF11-specific immunoassay development, SMAD2/3 phosphorylation assays, myoblast differentiation assays, in vivo muscle regeneration assays Cell metabolism High 26001423
2017 Supraphysiological systemic overexpression of GDF11 (via AAV) causes substantial atrophy of skeletal and cardiac muscle in mice through activation of p-SMAD2/3 and the ubiquitin-proteasome pathway. GDF11 and myostatin activate p-SMAD2/3 with similar potency and induce comparable myotube atrophy in vitro. Greater cardiac expression of TGFβR1 may explain GDF11-specific cardiac phenotype. AAV-mediated systemic overexpression, in vitro myoblast culture assays, p-SMAD2/3 measurement, muscle mass and function measurement EMBO molecular medicine High 28270449
2017 PCSK5 (proprotein convertase subtilisin/kexin type 5) is required for GDF11 processing and bioactivation in triple-negative breast cancer (TNBC) cells. PCSK5 deficiency causes inactive GDF11 precursor to accumulate intracellularly. PCSK5 reconstitution mobilizes this latent GDF11 reservoir and suppresses TNBC metastasis, establishing GDF11 as a tumor suppressor inactivated by precursor sequestration. PCSK5 reconstitution in TNBC cells, 3D culture invasion assays, intraductal xenograft model, Western blot for GDF11 precursor vs. mature forms, lung metastasis quantification Developmental cell High 29161592
2016 GDF11 inhibits bone formation by inducing SMAD2/3 phosphorylation, which represses Runx2 expression in bone marrow mesenchymal stem cells, inhibiting osteoblastic differentiation in vitro and accelerating age-related bone loss in vivo. GDF11 had no effect on osteoclast differentiation or bone resorption. In vitro osteoblast differentiation assays, SMAD2/3 phosphorylation assays, Runx2 expression analysis, intraperitoneal GDF11 injection in mice, bone histomorphometry Calcified tissue international Medium 27395058
2020 Gdf11 null mice exhibit reduced bone mass through impaired osteoblast and chondrocyte maturation and increased osteoclastogenesis, while Mstn null mice display the opposite (enhanced bone mass). Mechanistically, Mstn deletion upregulates Gdf11 expression, which activates BMP signaling to enhance osteogenesis, establishing GDF11 as a pro-osteogenic factor opposing MSTN. Gdf11-/- and Mstn-/- genetic mouse models, bone mass measurement, osteoblast/chondrocyte differentiation assays, BMP signaling analysis, FST-overexpressing mouse analysis Proceedings of the National Academy of Sciences of the United States of America High 32071240
2017 GDF11 secreted from the posterior axial mesoderm integrates sacral vertebrae and hindlimb positioning by inducing Hox gene expression in two different primordia (somites and lateral plate mesoderm). Manipulating the onset of GDF11 activity in chicken embryos altered hindlimb position; comparative analysis showed that heterochronic shifts in Gdf11 expression onset correlate with evolutionary diversity of hindlimb positioning. Manipulation of GDF11 activity onset in chick embryos, comparative embryo analysis, Hox gene expression assays Nature ecology & evolution Medium 29046533
2018 GDF11 modulates intracellular Ca2+ signaling via the IP3 pathway in neonatal cardiomyocytes, and this Ca2+ response is required for GDF11-induced Smad2/3 phosphorylation and transcriptional activity. Blocking IP3-dependent Ca2+ release abolishes GDF11-induced Smad2/3 activity. siRNA knockdown of Smad2 and Smad3 inhibits the antihypertrophic effects of GDF11. Intracellular Ca2+ imaging, IP3 pathway inhibitors, BAPTA-AM Ca2+ chelation, Smad2/3 luciferase reporter, siRNA knockdown, cardiomyocyte hypertrophy assays International journal of molecular sciences Medium 29783655
2016 GDF11 activates both Smad1/5/8 and Smad2/3 signaling pathways in human umbilical vein endothelial cells (HUVECs), and increases NADPH oxidase 4 (NOX4) protein expression and p-JNK and p-AMPK levels. GDF11 showed no significant effect on p38, ERK, or Akt signaling, and had no significant effect on HUVEC proliferation or migration. Western blot for phospho-signaling proteins, MTT cell viability assay, wound healing migration assay Oncotarget Medium 26919250
2019 GDF11 induces SMAD2/3 phosphorylation and nuclear translocation via ALK5 in hepatocellular carcinoma (HCC) cells but not in primary hepatocytes. ALK5 inhibition blocks GDF11-mediated SMAD2/3 signaling and attenuates lipid accumulation in HCC cells. Transcriptomics identified TGF-β and PI3K-AKT signaling as top pathways activated. Western blot for SMAD2/3 nuclear translocation, ALK5 inhibitor (SB431542), lipidomics, transcriptomics (RNA-seq), primary hepatocyte vs. HCC cell comparison Biochimica et biophysica acta. Molecular and cell biology of lipids Medium 33684566
2019 GDF11 inhibits hepatic hepcidin (HAMP) expression by decreasing BMP-SMAD signaling through enhancement of SMURF1-mediated ubiquitination and by activating ERK1/2 (MAPK3/1) signaling. ERK1/2 activation is required for GDF11- or SMURF1-mediated suppression of BMP-SMAD and HAMP expression. In vivo GDF11 administration, in vitro hepatocyte treatment, Western blot for BMP-SMAD and ERK signaling, SMURF1 expression assays British journal of haematology Medium 31418854
2019 Crystal structure of the WFIKKN2 follistatin domain (FSD) revealed that WFIKKN2 FSD binds both GDF8 and GDF11 and blocks their interaction with the type II receptor ActRIIB. Surface-exposed residues important for antagonism were identified by alanine scanning mutagenesis. The WFIKKN2 FSD uses different residues than follistatin or FSTL3 for ligand antagonism. Crystal structure determination (1.39 Å), native gel shift assay, surface plasmon resonance, alanine scanning mutagenesis The Journal of biological chemistry High 30814254
2009 BMP-11/GDF11 and myostatin maintain human embryonic stem cell (hESC) self-renewal under feeder-free conditions by activating SMAD2/3 phosphorylation through type I TGF-β receptors (ALK4/5/7). The type I TGF-β receptor inhibitor SB431542 completely blocked this maintenance activity. hESC culture assays, SMAD2/3 phosphorylation measurement, pharmacological inhibition (SB431542), pluripotency marker analysis Cloning and stem cells Medium 19751112
2019 GDF11 promotes human extravillous trophoblast (EVT) cell invasion by stimulating MMP2 expression via ALK4/5-SMAD2/3 signaling, which upregulates inhibitor of DNA-binding protein 2 (ID2), required for GDF11-stimulated MMP2 expression and invasion. siRNA knockdown of ALK4/5 and ID2, pharmacological inhibitors, Matrigel transwell invasion assay, Western blot Cell communication and signaling : CCS Medium 35705978
2020 GDF11 inhibits adipogenesis in pre-adipocytes via ALK5-SMAD2/3 activation in cooperation with the WNT/β-catenin pathway. WNT/β-catenin pathway inhibition results in adipogenic differentiation despite GDF11. GDF11 also increases adiponectin secretion and glucose uptake in mature adipocytes. ALK5 inhibitor, WNT pathway inhibitor, adipogenesis assays, glucose uptake assays, transcriptomics, ob/ob mouse in vivo experiments Cell proliferation Medium 35920128
2019 A loss-of-function GDF11 variant (p.Arg298Gln) at the Furin protease cleavage site was identified in a human family with cleft lip/palate and vertebral/rib abnormalities mirroring Gdf11 knockout mice. Functional assays demonstrated that this substitution significantly impairs GDF11 function, confirming GDF11 processing at the furin cleavage site is essential for human development. Exome sequencing, functional assays of mutant GDF11, zebrafish gdf11 loss-of-function model Human mutation Medium 31215115
2022 Pathophysiological levels of GDF11 activate Smad2/3 signaling in human iPSC-derived myocytes and induce muscle atrophy by upregulating the E3 ubiquitin ligase Atrogin-1 via FOXO1. FOXO1 blockade reverses GDF11-induced Atrogin-1 expression and atrophic phenotype, establishing a GDF11→Smad2/3→FOXO1→Atrogin-1 axis for muscle atrophy. Human iPSC-derived myocytes, Smad2/3 phosphorylation assays, FOXO1 inhibition, Atrogin-1 expression analysis, myocyte diameter measurement American journal of physiology. Cell physiology Medium 36094432
2020 GDF11 enhances mesenchymal stem cell (MSC) viability under hypoxia by activating TGF-β receptor/Smad2/3 signaling, which upregulates the mitochondrial protease YME1L. YME1L in turn promotes OPA1 processing, preserving mitochondrial fusion morphology. TGF-β receptor inhibitor (SB431542) or Smad2/3 inhibitor (SIS3) blocked these effects. Lentiviral GDF11 overexpression, pharmacological inhibitors of TGF-β receptor and Smad2/3, Western blot for YME1L and OPA1, mitochondrial morphology imaging, cardiac MSC transplantation Stem cells translational medicine Medium 32515551
2001 In chick limb, GDF11 negatively regulates both chondrogenesis and myogenesis; GDF11-soaked beads implanted into wing buds cause limb truncations and inhibit both cartilage and muscle. In vitro micromass assays confirmed inhibition of chondrogenic and myogenic differentiation. GDF11 also induces ectopic expression of Hoxd-11 and Hoxd-13, and induces expression of its own antagonist follistatin. Bead implantation in chick embryo wing buds, in vitro micromass differentiation assays, Hox gene expression analysis, follistatin expression assay Developmental biology Medium 11203700
2002 Recombinant GDF11 induces expression of dentin sialoprotein (Dsp), an odontoblast differentiation marker, in mouse dental papilla mesenchyme in organ culture. In vivo electroporation-mediated Gdf11 gene transfer stimulated reparative dentin formation during pulpal wound healing in canine teeth. Organ culture differentiation assay, electroporation-mediated gene transfer, in vivo gene delivery in dog dental pulp Gene therapy Medium 12040463
2019 GDF11 induces differentiation and apoptosis and suppresses migration of C17.2 neural stem cells. Phospho-proteomic profiling showed GDF11 significantly increases phosphorylation of p38, ERK, and Akt (MAPK pathway activation) in these cells. Phospho-proteome profiling array, Western blot validation, differentiation assays, apoptosis assays, migration assay PeerJ Medium 30202652
2019 GDF11 promotes the Smad2/3 signaling pathway to upregulate HOXA3, which acts as a transcriptional repressor of NLRP3 inflammasome expression (confirmed by ChIP assay), thereby inhibiting cardiomyocyte pyroptosis in myocardial infarction. AAV9-GDF11 overexpression in MI mice, PROMO/JASPAR prediction and ChIP assay for HOXA3 binding to NLRP3 promoter, Western blot for Smad2/3 pathway Cell death & disease Medium 33100331
2021 Endogenous GDF11 in the adult brain is most highly expressed in neurogenic niches. Inducible conditional knockout of Gdf11 during adulthood increased proliferation of neural progenitors but decreased newborn neurons in the hippocampus, confirming that endogenous GDF11 remains a negative regulator of adult hippocampal neurogenesis. Tamoxifen-inducible conditional knockout mouse, immunohistochemistry, neural progenitor proliferation and newborn neuron quantification Molecular brain High 34488822
2019 GDF11 treatment of GDF11-null kidney fibroblasts (NRK49f) induced their proliferation and activation, and promoted epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells (IMCD-3) in a SMAD3-dependent manner. Systemic high-dose GDF11 in adult mice caused renal fibrosis and failure associated with SMAD2 phosphorylation, which was blocked by follistatin. In vitro renal cell line assays, SMAD3-dependence assays (pharmacological), in vivo GDF11 injection with follistatin rescue, 5/6 nephrectomy model Surgery Medium 29731246
2019 GDF11 activates TGF-β/Smad2/3 and PI3K-AKT-FoxO1 signaling pathways in pancreatic beta-cells and adipose tissue to protect beta-cell function and survival. Anti-GDF11 monoclonal antibody treatment caused beta-cell failure, establishing an endogenous requirement for GDF11 signaling in beta-cell maintenance. Recombinant GDF11 supplementation, anti-GDF11 antibody neutralization, in vitro islet and MIN6 cell assays, signaling pathway analysis Diabetes Medium 28450417
2021 Endogenous GDF11 expressed in adult rat CNS is found in most neurons and their axons, as well as in astrocytes and ependymal cells, demonstrating widespread expression throughout the adult brain. Immunohistochemistry in adult rat CNS sections Journal of chemical neuroanatomy Low 29448002
2023 Systemic recombinant GDF11 delivery prior to myocardial ischemia-reperfusion in mice augmented infarct size by accelerating pro-apoptotic signaling. Targeted transcriptomics revealed attenuated Nkx2-5 expression in CD105+ cells with adjacent pro-apoptotic caspase-3 activity, suggesting an indirect apoptotic effect. In humans, circulating GDF11 levels increase with age and predict larger infarct size independently. Recombinant GDF11 delivery in mice, ischemia-reperfusion model, targeted transcriptomics, immunomapping, validated LC-MS/MS GDF11 assay in human MI patients Cardiovascular research Medium 37742057

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle. Science (New York, N.Y.) 677 24797481
2015 GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration. Cell metabolism 439 26001423
2003 Autoregulation of neurogenesis by GDF11. Neuron 276 12546816
2001 Assigning the positional identity of spinal motor neurons: rostrocaudal patterning of Hox-c expression by FGFs, Gdf11, and retinoids. Neuron 247 11754833
2005 GDF11 controls the timing of progenitor cell competence in developing retina. Science (New York, N.Y.) 191 15976303
2016 Biochemistry and Biology of GDF11 and Myostatin: Similarities, Differences, and Questions for Future Investigation. Circulation research 169 27034275
2002 Activin type IIA and IIB receptors mediate Gdf11 signaling in axial vertebral patterning. Genes & development 164 12414726
2004 GDF11 modulates NGN3+ islet progenitor cell number and promotes beta-cell differentiation in pancreas development. Development (Cambridge, England) 134 15548585
2005 GDF11 forms a bone morphogenetic protein 1-activated latent complex that can modulate nerve growth factor-induced differentiation of PC12 cells. Molecular and cellular biology 127 15988002
2017 Supraphysiological levels of GDF11 induce striated muscle atrophy. EMBO molecular medicine 101 28270449
2010 METABOLIC FUNCTIONS OF MYOSTATIN AND GDF11. Immunology, endocrine & metabolic agents in medicinal chemistry 100 21197386
2018 The GDF11-FTO-PPARγ axis controls the shift of osteoporotic MSC fate to adipocyte and inhibits bone formation during osteoporosis. Biochimica et biophysica acta. Molecular basis of disease 98 30279140
2017 Structural basis for potency differences between GDF8 and GDF11. BMC biology 97 28257634
2017 Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting. Basic research in cardiology 95 28647906
2016 GDF11 Protects against Endothelial Injury and Reduces Atherosclerotic Lesion Formation in Apolipoprotein E-Null Mice. Molecular therapy : the journal of the American Society of Gene Therapy 93 27502608
2015 Reduced Circulating GDF11 Is Unlikely Responsible for Age-Dependent Changes in Mouse Heart, Muscle, and Brain. Endocrinology 92 26372181
2011 Activin and GDF11 collaborate in feedback control of neuroepithelial stem cell proliferation and fate. Development (Cambridge, England) 91 21852401
2008 In vivo functions of the proprotein convertase PC5/6 during mouse development: Gdf11 is a likely substrate. Proceedings of the National Academy of Sciences of the United States of America 85 18378898
2016 Targeted myocardial delivery of GDF11 gene rejuvenates the aged mouse heart and enhances myocardial regeneration after ischemia-reperfusion injury. Basic research in cardiology 84 28004242
2020 Overexpression of circRNA circUCK2 Attenuates Cell Apoptosis in Cerebral Ischemia-Reperfusion Injury via miR-125b-5p/GDF11 Signaling. Molecular therapy. Nucleic acids 83 33230465
2013 Regulation of GDF-11 and myostatin activity by GASP-1 and GASP-2. Proceedings of the National Academy of Sciences of the United States of America 83 24019467
2006 The function of growth/differentiation factor 11 (Gdf11) in rostrocaudal patterning of the developing spinal cord. Development (Cambridge, England) 83 16790475
2002 Induction of dental pulp stem cell differentiation into odontoblasts by electroporation-mediated gene delivery of growth/differentiation factor 11 (Gdf11). Gene therapy 75 12040463
2001 Gdf11 is a negative regulator of chondrogenesis and myogenesis in the developing chick limb. Developmental biology 72 11203700
2017 Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer. Developmental cell 70 29161592
2022 GDF11 promotes wound healing in diabetic mice via stimulating HIF-1ɑ-VEGF/SDF-1ɑ-mediated endothelial progenitor cell mobilization and neovascularization. Acta pharmacologica Sinica 68 36347996
2009 Foxg1 promotes olfactory neurogenesis by antagonizing Gdf11. Development (Cambridge, England) 67 19297409
2020 GDF11 inhibits cardiomyocyte pyroptosis and exerts cardioprotection in acute myocardial infarction mice by upregulation of transcription factor HOXA3. Cell death & disease 66 33100331
2004 Stimulation of reparative dentin formation by ex vivo gene therapy using dental pulp stem cells electrotransfected with growth/differentiation factor 11 (Gdf11). Human gene therapy 65 15610605
2017 GDF11 Attenuates Development of Type 2 Diabetes via Improvement of Islet β-Cell Function and Survival. Diabetes 63 28450417
2019 Exogenous GDF11 attenuates non-canonical TGF-β signaling to protect the heart from acute myocardial ischemia-reperfusion injury. Basic research in cardiology 62 30900023
2020 GDF11 promotes osteogenesis as opposed to MSTN, and follistatin, a MSTN/GDF11 inhibitor, increases muscle mass but weakens bone. Proceedings of the National Academy of Sciences of the United States of America 61 32071240
2015 Growth and differentiation factor 11 (GDF11): Functions in the regulation of erythropoiesis and cardiac regeneration. Pharmacology & therapeutics 59 26523637
2011 Gdf11 facilitates temporal progression of neurogenesis in the developing spinal cord. The Journal of neuroscience : the official journal of the Society for Neuroscience 59 21248112
2018 GDF11 Improves Angiogenic Function of EPCs in Diabetic Limb Ischemia. Diabetes 57 30026260
2016 GDF11 improves tubular regeneration after acute kidney injury in elderly mice. Scientific reports 56 27703192
2019 The role of GDF11 in aging and skeletal muscle, cardiac and bone homeostasis. Critical reviews in biochemistry and molecular biology 49 31144559
2016 GDF11/BMP11 activates both smad1/5/8 and smad2/3 signals but shows no significant effect on proliferation and migration of human umbilical vein endothelial cells. Oncotarget 47 26919250
2005 The isolation, characterization, and expression of a novel GDF11 gene and a second myostatin form in zebrafish, Danio rerio. Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology 45 15886039
2018 GDF11 Rejuvenates Cerebrovascular Structure and Function in an Animal Model of Alzheimer's Disease. Journal of Alzheimer's disease : JAD 42 29480172
2017 Anatomical integration of the sacral-hindlimb unit coordinated by GDF11 underlies variation in hindlimb positioning in tetrapods. Nature ecology & evolution 39 29046533
2019 The influence of GDF11 on brain fate and function. GeroScience 37 30729414
2019 Systemic GDF11 stimulates the secretion of adiponectin and induces a calorie restriction-like phenotype in aged mice. Aging cell 36 31637864
2016 GDF11 Inhibits Bone Formation by Activating Smad2/3 in Bone Marrow Mesenchymal Stem Cells. Calcified tissue international 36 27395058
2011 Growing backwards: an inverted role for the shrimp ortholog of vertebrate myostatin and GDF11. The Journal of experimental biology 36 21795562
2021 GDF-11 Protects the Traumatically Injured Spinal Cord by Suppressing Pyroptosis and Necroptosis via TFE3-Mediated Autophagy Augmentation. Oxidative medicine and cellular longevity 34 34712387
2019 A GDF11/myostatin inhibitor, GDF11 propeptide-Fc, increases skeletal muscle mass and improves muscle strength in dystrophic mdx mice. Skeletal muscle 34 31133057
2019 Gdf11 gene transfer prevents high fat diet-induced obesity and improves metabolic homeostasis in obese and STZ-induced diabetic mice. Journal of translational medicine 34 31847906
2018 GDF11 antagonizes TNF-α-induced inflammation and protects against the development of inflammatory arthritis in mice. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 34 30407878
2021 GDF11 alleviates secondary brain injury after intracerebral hemorrhage via attenuating mitochondrial dynamic abnormality and dysfunction. Scientific reports 33 33597668
2022 GDF11 ameliorates severe acute pancreatitis through modulating macrophage M1 and M2 polarization by targeting the TGFβR1/SMAD-2 pathway. International immunopharmacology 32 35461108
2019 GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion. Biochimica et biophysica acta. Molecular basis of disease 32 30890427
2020 Anti-Aging Effects of GDF11 on Skin. International journal of molecular sciences 31 32283613
2020 GDF11 enhances therapeutic efficacy of mesenchymal stem cells for myocardial infarction via YME1L-mediated OPA1 processing. Stem cells translational medicine 31 32515551
2019 GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway. Inflammation 31 30259241
2014 Effective RNA-silencing strategy of Lv-MSTN/GDF11 gene and its effects on the growth in shrimp, Litopenaeus vannamei. Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology 30 25246367
2013 Direct activation of a mouse Hoxd11 axial expression enhancer by Gdf11/Smad signalling. Developmental biology 29 24016758
2021 PPARα Targeting GDF11 Inhibits Vascular Endothelial Cell Senescence in an Atherosclerosis Model. Oxidative medicine and cellular longevity 28 33728018
2021 GDF11 Alleviates Pathological Myocardial Remodeling in Diabetic Cardiomyopathy Through SIRT1-Dependent Regulation of Oxidative Stress and Apoptosis. Frontiers in cell and developmental biology 28 34262905
2018 GDF11 Modulates Ca2+-Dependent Smad2/3 Signaling to Prevent Cardiomyocyte Hypertrophy. International journal of molecular sciences 28 29783655
2020 Hypoxia-induced miR-1260b regulates vascular smooth muscle cell proliferation by targeting GDF11. BMB reports 27 31818357
2013 cDNA cloning and expression analysis of myostatin/GDF11 in shrimp, Litopenaeus vannamei. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology 27 23402749
2013 Transcriptional basis for the inhibition of neural stem cell proliferation and migration by the TGFβ-family member GDF11. PloS one 27 24244313
2020 Candidate rejuvenating factor GDF11 and tissue fibrosis: friend or foe? GeroScience 26 33025411
2019 GDF11 Implications in Cancer Biology and Metabolism. Facts and Controversies. Frontiers in oncology 26 31681577
2007 Characterization of amphioxus GDF8/11 gene, an archetype of vertebrate MSTN and GDF11. Development genes and evolution 25 17551751
2023 Circulating GDF11 exacerbates myocardial injury in mice and associates with increased infarct size in humans. Cardiovascular research 24 37742057
2021 GDF11 rapidly increases lipid accumulation in liver cancer cells through ALK5-dependent signaling. Biochimica et biophysica acta. Molecular and cell biology of lipids 23 33684566
2019 Mutations in GDF11 and the extracellular antagonist, Follistatin, as a likely cause of Mendelian forms of orofacial clefting in humans. Human mutation 23 31215115
2018 GDF11 expression in the adult rat central nervous system. Journal of chemical neuroanatomy 23 29448002
2022 GDF11 inhibits adipogenesis and improves mature adipocytes metabolic function via WNT/β-catenin and ALK5/SMAD2/3 pathways. Cell proliferation 22 35920128
2018 GDF11 restrains tumor growth by promoting apoptosis in pancreatic cancer. OncoTargets and therapy 22 30568460
2009 BMP-11 and myostatin support undifferentiated growth of human embryonic stem cells in feeder-free cultures. Cloning and stem cells 22 19751112
2019 Neuroprotective potential of GDF11 in experimental intracerebral hemorrhage in elderly rats. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 21 30827882
2018 GDF11 induces kidney fibrosis, renal cell epithelial-to-mesenchymal transition, and kidney dysfunction and failure. Surgery 21 29731246
2020 Exogenous GDF11, but not GDF8, reduces body weight and improves glucose homeostasis in mice. Scientific reports 20 32165710
2018 Late-onset administration of GDF11 extends life span and delays development of age-related markers in the annual fish Nothobranchius guentheri. Biogerontology 20 30519861
2011 PCSK5 and GDF11 expression in the hindgut region of mouse embryos with anorectal malformations. European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift fur Kinderchirurgie 20 21480163
2022 GDF-11 promotes human trophoblast cell invasion by increasing ID2-mediated MMP2 expression. Cell communication and signaling : CCS 19 35705978
2022 GDF11 inhibits abnormal adipogenesis of condylar chondrocytes in temporomandibular joint osteoarthritis. Bone & joint research 19 35787089
2021 Heterozygous loss-of-function variants significantly expand the phenotypes associated with loss of GDF11. Genetics in medicine : official journal of the American College of Medical Genetics 19 34113007
2019 Lymphatic endothelium contributes to colorectal cancer growth via the soluble matrisome component GDF11. International journal of cancer 19 30889293
2019 Growth differentiation factor 11 (GDF11) has pronounced effects on skin biology. PloS one 19 31181098
2018 GDF11 induces differentiation and apoptosis and inhibits migration of C17.2 neural stem cells via modulating MAPK signaling pathway. PeerJ 19 30202652
2016 Questions and Answers About Myostatin, GDF11, and the Aging Heart. Circulation research 19 26837737
2023 Hydrogen sulfide antagonizes formaldehyde-induced ferroptosis via preventing ferritinophagy by upregulation of GDF11 in HT22 cells. Toxicology 18 37105376
2020 Chondrocyte suppression is mediated by miR-129-5p via GDF11/SMAD3 signaling in developmental dysplasia of the hip. Journal of orthopaedic research : official publication of the Orthopaedic Research Society 18 32396235
2020 GDF11 restricts aberrant lipogenesis and changes in mitochondrial structure and function in human hepatocellular carcinoma cells. Journal of cellular physiology 18 33174245
2019 Analysis of Cre-mediated genetic deletion of Gdf11 in cardiomyocytes of young mice. American journal of physiology. Heart and circulatory physiology 18 31125255
2019 GDF11 contributes to hepatic hepcidin (HAMP) inhibition through SMURF1-mediated BMP-SMAD signalling suppression. British journal of haematology 18 31418854
2016 Elevated GDF11 Is a Risk Factor for Age-Related Frailty and Disease in Humans. Cell metabolism 18 27411004
2024 GDF11 OVEREXPRESSION ALLEVIATES SEPSIS-INDUCED LUNG MICROVASCULAR ENDOTHELIAL BARRIER DAMAGE BY ACTIVATING SIRT1/NOX4 SIGNALING TO INHIBIT FERROPTOSIS. Shock (Augusta, Ga.) 17 38920138
2022 Pathophysiological levels of GDF11 activate Smad2/Smad3 signaling and induce muscle atrophy in human iPSC-derived myocytes. American journal of physiology. Cell physiology 17 36094432
2020 GDF11 induces mild hepatic fibrosis independent of metabolic health. Aging 17 33126224
2021 GDF11 prevents the formation of thoracic aortic dissection in mice: Promotion of contractile transition of aortic SMCs. Journal of cellular and molecular medicine 16 33764670
2019 Crystal structure of the WFIKKN2 follistatin domain reveals insight into how it inhibits growth differentiation factor 8 (GDF8) and GDF11. The Journal of biological chemistry 16 30814254
2019 MiR-92a regulates endothelial progenitor cells (EPCs) by targeting GDF11 via activate SMAD2/3/FAK/Akt/eNOS pathway. Annals of translational medicine 16 31807544
2021 GDF11 expressed in the adult brain negatively regulates hippocampal neurogenesis. Molecular brain 15 34488822
2020 GDF11 replenishment protects against hypoxia-mediated apoptosis in cardiomyocytes by regulating autophagy. European journal of pharmacology 15 32861661
2017 Modulation of GDF11 expression and synaptic plasticity by age and training. Oncotarget 15 28938532

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