Affinage

TXNRD2

Thioredoxin reductase 2, mitochondrial · UniProt Q9NNW7

Length
524 aa
Mass
56.5 kDa
Annotated
2026-06-10
46 papers in source corpus 16 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TXNRD2 encodes a mitochondrial thioredoxin reductase that constitutes the upstream node of the mitochondrial thioredoxin antioxidant system, scavenging mitochondrial ROS and reactive nitrogen species to protect organelle integrity and metabolic function (PMID:26199228, PMID:33579817). Its catalytic activity depends on a conserved FAD-binding domain and C-terminal homodimerization; disease-associated missense and splice mutations that disrupt these features abolish enzymatic activity and act dominant-negatively (PMID:21247928, PMID:39097530). TXNRD2 operates upstream of thioredoxin-2 and peroxiredoxin-3 (Prx3) to eliminate mitochondrial H2O2, and loss of function oxidizes Prx3 and raises mitochondrial ROS and peroxynitrite, dysregulating protein tyrosine phosphorylation, nitration, and cell-cycle progression (PMID:12705894, PMID:33579817, PMID:38513765). Through this redox control TXNRD2 is required for cardiac mitochondrial integrity, autophagic flux, and energy metabolism—its cardiac-specific loss causes dilated cardiomyopathy with mitochondrial degeneration and HIF-1α stabilization (PMID:26199228)—and for adrenocortical redox homeostasis and glucocorticoid/cortisol production, with human loss-of-function alleles causing adrenal failure (PMID:24601690, PMID:39097530). Its activity is positively regulated by direct binding of p53R2 and its expression is a target of Wnt/β-catenin signaling (PMID:27866984, PMID:22683372), and activating lysine-340 lactylation by AARS2 enhances mitochondrial TrxR activity to promote mitophagy and ferroptosis resistance (PMID:41704008).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2002 Low

    Defining the gene architecture established TrxR2 as a homodimeric enzyme and revealed a splice variant predicted to alter the dimerization interface, framing later structure-function work.

    Evidence Genomic sequencing, intron-exon mapping, and RT-PCR of mouse TrxR2

    PMID:12132591

    Open questions at the time
    • Functional consequence of the intron-14-lacking splice variant was not experimentally tested
    • No biochemical demonstration of altered dimer conformation
  2. 2003 Medium

    Dominant-negative disruption showed TrxR2 is an active component of the mitochondrial H2O2-eliminating system that constrains redox-dependent signaling and proliferation.

    Evidence Tetracycline-regulated dominant-negative TrxR2 in HeLa cells with ROS, phosphotyrosine/ERK, and cell-cycle readouts

    PMID:12705894

    Open questions at the time
    • Dominant-negative effects not confirmed against clean genetic loss
    • Direct substrate relationship with Trx2/Prx3 inferred, not biochemically reconstituted here
  3. 2004 Medium

    Testing whether excess enzyme is protective showed overexpression does not regulate mitochondria-dependent apoptosis, indicating TrxR2 is not rate-limiting for cell-death decisions under these conditions.

    Evidence Stable EGFP-TrxR2 overexpression with enzymatic activity, mitochondrial fractionation, and apoptosis flow cytometry in Neuro2A cells

    PMID:15082714

    Open questions at the time
    • Negative result limited to overexpression in one cell type
    • Does not address loss-of-function consequences for apoptosis
  4. 2007 Medium

    Gene-dosage analysis established that TrxR2 enzymatic activity scales with gene copy and interacts with selenium availability tissue-specifically.

    Evidence Hemizygous mouse model with dietary selenium manipulation and tissue enzymatic activity assays

    PMID:17937623

    Open questions at the time
    • Phenotypic consequences of dose reduction not assessed
    • Mechanism of tissue-specific Se additivity unexplained
  5. 2011 High

    Disease-mutation reconstitution localized catalytic essentiality to the FAD-binding domain and demonstrated a dominant-negative mechanism linking TXNRD2 to dilated cardiomyopathy.

    Evidence Reconstitution of DCM-associated mutants in Txnrd2-/- fibroblasts with enzymatic and oxidative-stress survival assays

    PMID:21247928

    Open questions at the time
    • Causality in human DCM rests on association plus cellular dominant-negative effect
    • Structural basis of FAD-domain disruption not crystallographically defined
  6. 2012 Medium

    Identifying TXNRD2 as a Wnt/β-catenin target connected its expression to proliferative epithelial compartments.

    Evidence Wnt3a/APC cell models, crypt-villus fractionation, and inducible β-catenin knockout with RT-PCR and Western blot

    PMID:22683372

    Open questions at the time
    • Direct β-catenin/TCF occupancy at the TXNRD2 locus not demonstrated
    • Functional importance of Wnt-driven expression for crypt biology untested
  7. 2014 High

    A human stop-gain null allele established TXNRD2 as required for adrenocortical redox homeostasis and glucocorticoid production.

    Evidence Whole-exome sequencing plus shRNA knockdown in H295R adrenocortical cells with redox assays

    PMID:24601690

    Open questions at the time
    • Mechanistic link between redox imbalance and steroidogenic failure not detailed here
    • Single family genetic evidence
  8. 2015 High

    Adult cardiac-specific knockout demonstrated TrxR2 is required in vivo for mitochondrial integrity, autophagic flux, and energy metabolism, recapitulating dilated cardiomyopathy.

    Evidence Tamoxifen-inducible cardiac Cre/loxP knockout with echocardiography, electron microscopy, respirometry, and metabolomics

    PMID:26199228

    Open questions at the time
    • Whether autophagic accumulation is protective or pathological not resolved
    • Upstream trigger linking ROS to HIF-1α stabilization not defined
  9. 2016 Medium

    Two studies extended the activity axis: p53R2 was shown to directly bind and stimulate TrxR2 activity, and TrxR2 loss was shown to drive ROS-dependent chondrogenic differentiation and proliferation.

    Evidence Co-IP/pulldown and in vitro enzymatic assays with p53R2 KD/OE; shRNA knockdown in ATDC5 cells with NAC rescue

    PMID:27107686 PMID:27866984

    Open questions at the time
    • p53R2 interaction from a single lab without reciprocal in vivo validation
    • Structural basis of p53R2-mediated activation unknown
  10. 2021 High

    Endothelial-specific deletion established TrxR2 as a regulator of the NO/peroxynitrite balance, with mitochondrial peroxynitrite driving vascular and renal pathology.

    Evidence Endothelial conditional knockout with fluorescein-boronate/MitoPY1 probes, Prx3 redox state, nitration assays, and Mn(III)TMPyP rescue

    PMID:33579817

    Open questions at the time
    • Direct enzymatic handling of peroxynitrite versus indirect via Trx2/Prx3 not separated
    • Tissue specificity of vascular versus renal effects unresolved
  11. 2022 Medium

    Transgenic overexpression positioned TrxR2 as a rate-limiting enzyme of the mitochondrial thioredoxin system that enhances TCA/ETC function and systemic metabolism.

    Evidence Transgenic overexpression mice with glucose tolerance testing and mitochondrial/TCA/ETC activity assays

    PMID:35577894

    Open questions at the time
    • Molecular link between thioredoxin reduction and ETC enhancement not defined
    • Single overexpression model
  12. 2024 High

    Two studies localized TXNRD2 upstream of Trx2/Prx3 in suppressing ER stress and lipid peroxidation, and confirmed FAD-binding/dimerization as the enzymatically critical features in a patient adrenal cell model.

    Evidence siRNA knockdown in rat ICH model with selenium rescue; patient iPSC-derived adrenal-like cells carrying a C-terminal splice variant with steroidogenesis and ROS assays

    PMID:38513765 PMID:39097530

    Open questions at the time
    • ER stress link from single in vivo KD model (Medium)
    • Direct biochemical demonstration of impaired dimerization for the splice variant not shown
  13. 2026 Medium

    Identification of AARS2-mediated K340 lactylation revealed a post-translational activating modification that couples TrxR2 to mitophagy and ferroptosis resistance in cardiac microvasculature.

    Evidence Endothelial KO and transgenic mice, mass-spectrometry lactylation site mapping, custom lactylation antibody, and mitophagy/ferroptosis assays

    PMID:41704008

    Open questions at the time
    • SCP2/ACSL4/TUFM mechanistic chain from single lab
    • Stoichiometry and regulation of K340 lactylation in vivo not quantified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TrxR2's distinct functional outputs—peroxynitrite handling, ER-stress suppression, metabolic regulation, and lactylation-driven mitophagy—are coordinated, and the structural basis of its activation by p53R2, remain unresolved.
  • No structural model of the p53R2-TrxR2 complex
  • Tissue-specific selection among redox outputs not mechanistically explained
  • Direct substrate spectrum beyond Trx2 not enumerated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016491 oxidoreductase activity 4 GO:0140098 catalytic activity, acting on RNA 3
Localization
GO:0005739 mitochondrion 3
Pathway
R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-1430728 Metabolism 2
Partners
AARS2PRDX3RRM2BTXN2

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2004 EGFP-TrxR2 fusion protein is enzymatically active as a thioredoxin reductase and localizes to mitochondria when overexpressed in Neuro2A cells; overexpression of TrxR2 up to 6-fold did not protect cells against apoptotic stimuli (prooxidant or non-oxidant) nor prevent mitochondrial membrane potential dissipation, ROS induction, or caspase activation, indicating that excess TrxR2 does not regulate mitochondria-dependent apoptosis. Stable transfection of EGFP-TrxR2 fusion, enzymatic activity assay, mitochondrial fractionation, flow cytometry for apoptosis markers The Journal of biological chemistry Medium 15082714
2003 A dominant-negative form of TrxR2 (TrxR2DN) in HeLa cells caused increased hydrogen peroxide production upon EGF stimulation, elevated protein tyrosine phosphorylation of ERK and other proteins, and accelerated G1-to-S phase cell cycle progression and cell proliferation, establishing TrxR2 as a component of the mitochondrial H2O2-eliminating system (together with Prxm III and Trx2) that regulates protein tyrosine phosphorylation and cell growth. Tetracycline-off dominant-negative stable cell line, ROS measurement (H2O2), immunoblot for phosphotyrosine/ERK, flow cytometry for cell cycle Biochemical and biophysical research communications Medium 12705894
2011 Two DCM-associated TXNRD2 missense mutations (Ala59Thr and Gly375Arg) affect conserved residues in helices of the FAD-binding domain; neither mutant restored TrxR2 function in Txnrd2-/- mouse fibroblasts, and both exerted dominant-negative effects impairing survival of wild-type cells under oxidative stress, defining the FAD-binding domain as essential for enzymatic activity. Sequencing, reconstitution in Txnrd2-/- mouse fibroblasts, functional enzymatic assay, oxidative stress survival assay European heart journal High 21247928
2015 Heart-specific, tamoxifen-inducible knockout of Txnrd2 in adult mice leads to dilated cardiomyopathy with decreased fractional shortening and ejection fraction, mitochondrial degeneration, accumulation of autophagic bodies, elevated LAMP1/LC3-I/p62, reduced mitochondrial oxygen consumption, increased mitochondrial ROS, and HIF-1α stabilization, establishing Txnrd2 as required for mitochondrial integrity, autophagic flux, and energy metabolism in the aging heart. Conditional cardiac-specific Cre/loxP knockout, echocardiography, electron microscopy, mitochondrial oxygen consumption assay, metabolomics, Western blot Journal of the American Heart Association High 26199228
2014 A homozygous stop-gain mutation (p.Y447X) in TXNRD2 causes complete absence of TXNRD2 protein (confirmed by Western blot) and impairs redox homeostasis in a human adrenocortical cell line (H295R TXNRD2-knockdown), establishing TXNRD2 as required for adrenocortical redox homeostasis and glucocorticoid production in humans. Whole-exome sequencing, Sanger sequencing, RT-PCR, Western blot, shRNA knockdown in H295R cells, redox assay The Journal of clinical endocrinology and metabolism High 24601690
2016 p53R2 directly binds TrxR2 (shown by co-immunoprecipitation and pulldown), stimulates TrxR2 enzymatic activity in vitro, and is required for full TrxR2 activity in cells: TrxR2 activity is lower in p53R2-knockdown cells and higher upon p53R2 overexpression, in a p53-independent manner; p53R2 knockdown also suppresses UV-induced TrxR activity. Co-immunoprecipitation, direct interaction assay, in vitro TrxR enzymatic activity assay, siRNA knockdown, overexpression Biochemical and biophysical research communications Medium 27866984
2021 Endothelial-specific deletion of Txnrd2 in mice increases steady-state peroxynitrite levels (measured by fluorescein-boronate probe) in vascular endothelial cells and vessels, elevates protein tyrosine nitration, oxidizes Prx3, and causes increased vascular stiffness, vascular wall hypertrophy, and renal pathology (glomerulosclerosis, Bowman's capsule thickening); peroxynitrite is generated in mitochondria (MitoPY1 probe) and peroxynitrite-decomposition catalyst Mn(III)TMPyP blunted the intravascular peroxynitrite. This establishes TrxR2 as regulator of the nitric oxide/peroxynitrite balance in endothelium. Endothelial-specific conditional knockout, redox-sensitive fluorescent probes (fluorescein-boronate, MitoPY1), protein nitration assay, redox state of Prx3, pharmacological rescue with Mn(III)TMPyP Proceedings of the National Academy of Sciences of the United States of America High 33579817
2002 The mouse TrxR2 gene spans 53 kb with 18 exons; an alternative splice variant lacking intron 14 produces a protein with a shorter interface domain, predicted to enable a heterodimeric or small-subunit homodimeric conformation, expanding the known homodimeric structure of TrxR2. Genomic sequencing, intron–exon mapping, RT-PCR identification of splice variant, structural prediction Molecules and cells Low 12132591
2012 TrxR2 (and GPx2 and TrxR3) expression is dependent on Wnt/β-catenin pathway activity in intestinal epithelium: expression is higher in proliferative crypt compartments where Wnt is active, is consistent with activated versus inhibited Wnt pathway in cell culture models, and is reduced by inducible knockout of β-catenin in colonic crypt base cells ex vivo, identifying TrxR2 as a novel Wnt target selenoprotein. Cell culture models with Wnt3a overexpression and APC-mediated inhibition, intestinal crypt/villus fractionation, inducible β-catenin knockout, RT-PCR and Western blot Biochimica et biophysica acta Medium 22683372
2016 TrxR2 deficiency in chondrogenic ATDC5 cells (via shRNA) increases mitochondrial ROS without altering mitochondrial membrane potential or ATP, enhances chondrogenic differentiation (elevated collagen II, aggrecan, GAG accumulation, mineralization), activates Akt signaling required for chondrogenesis, promotes cell cycle progression (increased S and G2/M phase), and induces apoptosis. NAC (antioxidant) reversed all these effects, placing mitochondrial ROS downstream of TrxR2 loss as the mechanistic driver. shRNA knockdown, ROS measurement, mitochondrial membrane potential assay, ATP assay, chondrogenic differentiation markers (qPCR, staining), flow cytometry (cell cycle, apoptosis), NAC rescue Experimental cell research Medium 27107686
2022 Transgenic mice overexpressing TrxR2 show enhanced glucose tolerance, decreased fat deposition on high-fat diet, and increased mitochondrial function driven by enhanced tricarboxylic acid cycle and electron transport chain function, establishing TrxR2 as a rate-limiting enzyme in the mitochondrial thioredoxin system that regulates mitochondrial metabolic function. Transgenic mouse overexpression, metabolic phenotyping (glucose tolerance test), mitochondrial function assays, TCA/ETC activity measurements Communications biology Medium 35577894
2024 Txnrd2 knockdown (siRNA) in a rat intracerebral hemorrhage model increases lipid peroxidation and ER stress (Trx2 and Prx3 pathway disrupted), worsens brain edema and neurological deficits. Pharmacological selenium (sodium selenite) restores Txnrd2 expression, inhibits ER stress markers, and reduces ROS via the Trx2/Prx3 pathway, positioning Txnrd2 upstream of Trx2/Prx3 in the mitochondrial antioxidant cascade controlling neuronal ER stress. siRNA knockdown in vivo (rat ICH model), selenium supplementation rescue, lipid peroxidation assay, ER stress protein expression, neurological deficit scoring Neuroscience Medium 38513765
2024 A homozygous TXNRD2 splice variant (c.1348-1G>T) produces a shorter protein lacking the C-terminus, affecting homodimerization and FAD-binding. Patient-derived induced pluripotent stem cell-derived adrenal-like cells (iALC) with this variant show loss of cortisol production, diminished overall adrenal steroidogenesis, and significantly increased ROS production, directly linking TXNRD2 enzymatic activity (FAD-binding and dimerization) to adrenal ROS detoxification and steroidogenesis. Whole exome sequencing, RNA analysis, protein structure modeling, iPS-cell-derived adrenal-like cells, cortisol and steroidogenesis assays, ROS measurement European journal of endocrinology High 39097530
2026 Endothelial-specific TrxR2 knockout exacerbates cardiac microvascular dysfunction and diabetic cardiomyopathy; TrxR2 inhibits mitochondria-associated ferroptosis by facilitating SCP2 degradation and blocking mitochondrial translocation of ACSL4 via mitophagy; TrxR2 maintains TUFM expression by scavenging oxygen radicals, enabling mitochondrial AMPK translocation for mitophagy activation. TrxR2 undergoes lactylation at lysine 340, mediated by mitochondrial AARS2; this modification enhances mitoTrxR activity and promotes mitophagy, conferring ferroptosis resistance. Endothelial-specific knockout mice, transgenic overexpression, mass spectrometry (lactylation site identification), custom lactylation antibody, bulk RNA-sequencing, fluorescence staining for mitoTrxR activity and lipid peroxyl radicals, mitophagy assays Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 41704008
2007 Txnrd2 hemizygosity (+/-) in mice reduces TrxR2 enzymatic activity in a gene-dose-dependent manner across all tissues examined; selenium depletion further reduces activity but not below levels seen with Se depletion alone, except in kidney, heart, and muscle where hemizygosity and Se depletion have an additive effect on TrxR2 activity. Hemizygous mouse model, selenium dietary manipulation, tissue Se content measurement, enzymatic activity assay across multiple tissues Biological chemistry Medium 17937623
2025 Non-covalent TXNRD inhibitors inhibit both TXNRD1 and TXNRD2 enzymatic activity; dual inhibition of TXNRD1 and TXNRD2 is more effective in suppressing TNBC cell growth than inhibiting either alone; the primary anti-cancer mechanism is depletion of endogenous deoxynucleotide pools and impairment of ribonucleotide reductase activity leading to G1 arrest, not the pro-oxidant effect, as exogenous deoxynucleotide supplementation restores cell viability and cycle progression. TXNRD1/2 dual inhibition with non-covalent inhibitors, transcriptomics, cell viability assay, cell cycle analysis, deoxynucleotide rescue experiment, TNBC xenograft in vivo bioRxivpreprint Medium bio_10.1101_2025.09.04.674327

Source papers

Stage 0 corpus · 46 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2016 Genome-wide association analysis identifies TXNRD2, ATXN2 and FOXC1 as susceptibility loci for primary open-angle glaucoma. Nature genetics 207 26752265
2014 Thioredoxin Reductase 2 (TXNRD2) mutation associated with familial glucocorticoid deficiency (FGD). The Journal of clinical endocrinology and metabolism 90 24601690
2004 Mitochondrial thioredoxin system: effects of TrxR2 overexpression on redox balance, cell growth, and apoptosis. The Journal of biological chemistry 90 15082714
2011 Mutations in the mitochondrial thioredoxin reductase gene TXNRD2 cause dilated cardiomyopathy. European heart journal 81 21247928
2017 Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity. Free radical biology & medicine 58 29080841
2021 The mitochondrial thioredoxin reductase system (TrxR2) in vascular endothelium controls peroxynitrite levels and tissue integrity. Proceedings of the National Academy of Sciences of the United States of America 54 33579817
2020 Wogonin induces cellular senescence in breast cancer via suppressing TXNRD2 expression. Archives of toxicology 52 32671444
2015 Heart-Specific Knockout of the Mitochondrial Thioredoxin Reductase (Txnrd2) Induces Metabolic and Contractile Dysfunction in the Aging Myocardium. Journal of the American Heart Association 50 26199228
2012 The selenoproteins GPx2, TrxR2 and TrxR3 are regulated by Wnt signalling in the intestinal epithelium. Biochimica et biophysica acta 49 22683372
2009 Over-expression of a human chromosome 22q11.2 segment including TXNRD2, COMT and ARVCF developmentally affects incentive learning and working memory in mice. Human molecular genetics 48 19617637
2013 SNP in TXNRD2 associated with radiation-induced fibrosis: a study of genetic variation in reactive oxygen species metabolism and signaling. International journal of radiation oncology, biology, physics 46 23597419
2016 GSK-3beta Inhibitor Induces Expression of Nrf2/TrxR2 Signaling Pathway to Protect against Renal Ischemia/Reperfusion Injury in Diabetic Rats. Kidney & blood pressure research 41 27924803
2003 Involvements of mitochondrial thioredoxin reductase (TrxR2) in cell proliferation. Biochemical and biophysical research communications 32 12705894
2012 Two thioredoxin reductases, trxr-1 and trxr-2, have differential physiological roles in Caenorhabditis elegans. Molecules and cells 29 22836943
2020 Prevalence and Genetic Diversity of Staphylococcal Enterotoxin (-Like) Genes sey, selw, selx, selz, sel26 and sel27 in Community-Acquired Methicillin-Resistant Staphylococcus aureus. Toxins 28 32456224
2022 Lipoxin A4 attenuates MSU-crystal-induced NLRP3 inflammasome activation through suppressing Nrf2 thereby increasing TXNRD2. Frontiers in immunology 27 36569930
2017 Inhibition of TrxR2 suppressed NSCLC cell proliferation, metabolism and induced cell apoptosis through decreasing antioxidant activity. Life sciences 25 28414076
2018 Smart mitochondrial-targeted cancer therapy: Subcellular distribution, selective TrxR2 inhibition accompany with declined antioxidant capacity. International journal of pharmaceutics 24 30500459
2015 Single nucleotide polymorphisms in the Trx2/TXNIP and TrxR2 genes of the mitochondrial thioredoxin antioxidant system and the risk of diabetic retinopathy in patients with Type 2 diabetes mellitus. Journal of diabetes and its complications 22 26763822
2016 TrxR2 deficiencies promote chondrogenic differentiation and induce apoptosis of chondrocytes through mitochondrial reactive oxygen species. Experimental cell research 21 27107686
2021 miR-195-5p exerts tumor-suppressive functions in human lung cancer cells through targeting TrxR2. Acta biochimica et biophysica Sinica 18 33332541
2022 Mitochondrial TrxR2 regulates metabolism and protects from metabolic disease through enhanced TCA and ETC function. Communications biology 17 35577894
2015 Association of thioredoxin reductase 2 (TXNRD2) gene polymorphisms with myocardial infarction in Slovene patients with type 2 diabetes mellitus. Diabetes research and clinical practice 17 25703281
2007 Effect of selenium on thioredoxin reductase activity in Txnrd1 or Txnrd2 hemizygous mice. Biological chemistry 17 17937623
2002 Genomic organization and identification of a novel alternative splicing variant of mouse mitochondrial thioredoxin reductase (TrxR2) gene. Molecules and cells 17 12132591
2023 Mitochondrial TXNRD2 and ME3 Genetic Risk Scores Are Associated with Specific Primary Open-Angle Glaucoma Phenotypes. Ophthalmology 12 36813040
2020 Synthesis of mitochondria-targeted coumarin-3-carboxamide fluorescent derivatives: Inhibiting mitochondrial TrxR2 and cell proliferation on breast cancer cells. Bioorganic & medicinal chemistry letters 12 33340662
2018 The study on polymorphisms of Sep15 and TrxR2 and the expression of AP-1 signaling pathway in Kashin-Beck disease. Bone 12 29653292
2008 [Association of genetic polymorphisms in selenoprotein GPX1 and TXNRD2 with genetic susceptibility of gastric cancer]. Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 12 19035188
2016 p53R2 regulates thioredoxin reductase activity through interaction with TrxR2. Biochemical and biophysical research communications 10 27866984
2024 Txnrd2 Attenuates Early Brain Injury by Inhibition of Oxidative Stress and Endoplasmic Reticulum Stress via Trx2/Prx3 Pathway after Intracerebral Hemorrhage in Rats. Neuroscience 9 38513765
2019 TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt-Parkin pathway. Toxicology research 7 31588341
2021 TXNRD2 (rs35934224) CT genotype as possible protective marker for primary open-angle glaucoma in a Brazilian population. Arquivos brasileiros de oftalmologia 6 34431894
2021 Lack of Association Between Polymorphisms in TXNRD2 and LMX1B and Primary Open-Angle Glaucoma in a Saudi Cohort. Frontiers in genetics 5 34408771
2025 Elevated serum levels of GPX4, NDUFS4, PRDX5, and TXNRD2 as predictive biomarkers for castration resistance in prostate cancer patients: an exploratory study. British journal of cancer 4 39900986
2024 Insight into the role of TXNRD2 in steroidogenesis through a novel homozygous TXNRD2 splice variant. European journal of endocrinology 3 39097530
2022 Synthesis of mitochondria-targeted menadione cation derivatives: Inhibiting mitochondrial thioredoxin reductase (TrxR2) and inducing apoptosis in MGC-803 cells. Bioorganic & medicinal chemistry letters 2 35085721
2021 Association analysis of variants rs35934224 in TXNRD2 and rs6478746 in LMX1B in primary angle-closure and pseudoexfoliation glaucoma. European journal of ophthalmology 2 34461764
2010 [TrxR2 gene polymorphisms may not be associated with the susceptibility to Kashin-Beck disease]. Nan fang yi ke da xue xue bao = Journal of Southern Medical University 2 20965815
2025 Case report and literature review: novel TXNRD2 compound heterozygous variants in familial glucocorticoid deficiency type 5. Frontiers in pediatrics 1 40726908
2026 TrxR2 Lactylation Facilitates Mitochondrial Protection and Endothelial Ferroptosis Resistance in Diabetic Cardiomyopathy. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 0 41704008
2026 TRXR2, a thioredoxin reductase-encoding gene, contributes to protection against the oxidative stress and virulence in Scedosporium apiospermum. Microbial pathogenesis 0 42000058
2025 Diisononyl phthalate down-regulates the expression of antioxidant genes NFE2L2, TXN, and TXNRD2, while diethyl-hexyl terephthalate up-regulates their expression including SOD-1. Xenobiotica; the fate of foreign compounds in biological systems 0 40238463
2025 The bidirectional regulatory effect of TXNRD2 methylation in patients with chronic heart failure and its nonlinear dose-response relationship with key clinical parameters. Journal of cardiothoracic surgery 0 40468356
2025 The methylation of TXNRD2 with chronic heart failure: the interaction effect between methylation regulation and clinical parameters-- a single center pilot study. BMC cardiovascular disorders 0 40841993
2021 Erratum: Expression of concern: TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt-Parkin pathway. Toxicology research 0 34136125

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