| 2010 |
Piezo1 (Fam38A) is an essential component of a mechanically activated (MA) cation channel. RNA interference knockdown of Piezo1 eliminated rapidly adapting MA currents in a mouse neuroblastoma cell line, and overexpression of mouse Piezo1 induced a kinetically distinct MA current, establishing Piezo1 as a pore-forming component of an MA cation channel. |
RNAi knockdown, overexpression, whole-cell and outside-out patch-clamp electrophysiology |
Science |
High |
20813920
|
| 2011 |
The peptide GsMTx4 reversibly inhibits Piezo1-mediated mechanically activated currents in outside-out and whole-cell configurations, acting as a gating modifier (voltage-insensitive, active on closed channels) that shifts the pressure-gating curve ~30 mmHg rightward, with KD ~155 nM. The d-enantiomer was equally effective, consistent with membrane-mediated inhibition rather than stereospecific binding. |
Outside-out and whole-cell patch-clamp electrophysiology in HEK293 cells overexpressing Piezo1; kinetic rate-constant analysis |
Biochemistry |
High |
21696149
|
| 2010 |
Fam38A/Piezo1 localizes to the endoplasmic reticulum (ER) and activates integrin-ligand affinity by recruiting the small GTPase R-Ras to the ER, which increases Ca2+ release from cytoplasmic stores, activates calpain, and leads to talin cleavage. siRNA knockdown of Fam38A inactivates β1 integrin and reduces cell adhesion; this pathway is blocked by inhibition of R-Ras, calpain, or talin knockdown. |
siRNA knockdown, subcellular fractionation/immunofluorescence localization to ER, cell adhesion assays, pharmacological inhibition of R-Ras and calpain, co-immunoprecipitation |
Journal of Cell Science |
Medium |
20016066
|
| 2012 |
Gain-of-function mutations in PIEZO1 (FAM38A) cause hereditary xerocytosis (HX), an autosomal dominant hemolytic anemia with primary erythrocyte dehydration. PIEZO1 peptides were identified by discovery proteomics in human erythrocyte membranes, establishing Piezo1 as an endogenous erythrocyte membrane protein. |
Copy number analysis, linkage studies, exome sequencing, segregation analysis, discovery proteomics of erythrocyte membranes |
Blood |
High |
22529292
|
| 2014 |
Piezo1 is expressed in endothelial cells of developing blood vessels and is activated by shear stress. Endothelial-specific Piezo1 deletion is embryonic lethal with vascular remodeling defects, and loss of Piezo1 impairs shear-stress-induced stress fiber formation and cell orientation, linking Piezo1 mechanotransduction to regulation of endothelial cell morphology. |
Conditional endothelial-specific knockout mice, shear stress application, cell orientation and stress fiber assays, in vivo vascular phenotyping |
PNAS |
High |
24958852
|
| 2015 |
Yoda1, a synthetic small molecule identified by screening ~3.25 million compounds, acts as a chemical agonist for both human and mouse Piezo1, affecting sensitivity and inactivation kinetics of mechanically induced responses. Yoda1 activates purified Piezo1 channels reconstituted in artificial droplet lipid bilayers in the absence of other cellular components, demonstrating direct channel activation. |
Cell-based fluorescence screening, electrophysiology, reconstitution of purified Piezo1 in droplet lipid bilayers |
eLife |
High |
26001275
|
| 2015 |
Red blood cells exhibit Piezo1-dependent calcium entry in response to mechanical stretch. RBC-specific Piezo1 conditional knockout produces overhydrated, fragile RBCs. Piezo1 activation by Yoda1 causes calcium influx and subsequent RBC dehydration via downstream activation of the KCa3.1 Gardos channel, establishing the Piezo1→Gardos channel axis for RBC volume control. |
RBC-specific conditional knockout mice, calcium imaging, RBC fragility assays (in vitro and in vivo), Yoda1 pharmacology, Gardos channel pharmacological dissection |
eLife |
High |
26001274
|
| 2017 |
Mechanical stretch stimulates epithelial cell division through Piezo1. Stretch triggers cells paused in early G2 to activate calcium-dependent phosphorylation of ERK1/2, activating cyclin B transcription to drive mitosis. Piezo1 subcellular localization differs with cell density: in sparse (dividing) regions it localizes to the plasma membrane and cytoplasm, while in dense (extruding) regions it forms large cytoplasmic aggregates. |
Mechanical stretch of epithelia, calcium imaging, phospho-ERK assays, cyclin B reporter assays, Piezo1 knockdown, live-cell imaging of Piezo1 localization |
Nature |
High |
28199303
|
| 2019 |
Dietary fatty acids tune Piezo1 mechanical response: margaric acid (a saturated fatty acid) inhibits Piezo1 activation by increasing membrane bending stiffness, whereas polyunsaturated fatty acids (PUFAs) modulate channel inactivation by decreasing membrane bending stiffness. Fatty acid supplementation can abrogate gain-of-function Piezo1 mutation phenotypes. |
Lipid profiling, electrophysiology, atomic force microscopy membrane stiffness measurements, fatty acid supplementation in gain-of-function Piezo1 mutant cells |
Nature Communications |
High |
30867417
|
| 2019 |
Piezo1 is required for bone formation by osteoblasts: knockout of Piezo1 in osteoblast lineage cells disrupts osteogenesis and impairs bone structure and strength, and simulated microgravity suppresses Piezo1 expression in osteoblasts to reduce their function. |
Osteoblast-lineage-specific conditional knockout mice, bone histology and biomechanical testing, microgravity simulation, gene expression analysis |
eLife |
High |
31290742
|
| 2019 |
Piezo1 mediates fluid shear stress-induced gene expression changes in osteocytes, and conditional deletion of Piezo1 in osteoblasts and osteocytes reduces bone mass and strength. Administration of a Piezo1 agonist (Yoda1) to adult mice increases bone mass, mimicking mechanical loading. |
Fluid shear stress assays in cultured osteocytes, conditional knockout mice, in vivo Yoda1 administration, bone mass and strength measurements |
eLife |
High |
31588901
|
| 2019 |
Piezo1 activation leads to ATP release from cells, which acts as an autocrine/paracrine signal activating P2 purinergic receptors to regulate cell functions. Piezo1-mediated mechanotransduction thus couples mechanical stimulation to downstream purinergic signaling. |
ATP release assays, P2 receptor pharmacology, Piezo1 knockdown/activation experiments across multiple cell types |
Frontiers in Pharmacology |
Medium |
31780935
|
| 2020 |
Piezo1 in mature adipocytes mediates diet-induced adipogenesis by releasing adipogenic fibroblast growth factor 1 (FGF1) upon channel opening, which induces adipocyte precursor differentiation through activation of FGF receptor 1. Mice lacking Piezo1 in mature adipocytes show defective preadipocyte differentiation on high-fat diet. |
Mature adipocyte-specific conditional Piezo1 knockout mice, high-fat diet challenge, FGF1 measurement, FGFR1 pharmacological inhibition, adipogenesis assays |
Nature Communications |
High |
32385276
|
| 2020 |
Gut Piezo1 in enterochromaffin cells functions as a sensor for single-stranded RNA (ssRNA) from fecal microbiota, governing serotonin (5-HT) production. Intestinal epithelium-specific Piezo1 deletion profoundly disturbs gut peristalsis and suppresses serum 5-HT levels. Colonic infusion of RNase A suppressed gut motility and increased bone mass, confirming the ssRNA–Piezo1 axis. |
Intestinal epithelium-specific conditional Piezo1 knockout, fecal ssRNA identification as ligand, RNase A infusion experiments, calcium imaging, bone mass measurement |
Cell |
High |
32640190
|
| 2021 |
Piezo1 is a key regulator of macrophage phagocytic activity and erythrocyte turnover, controlling hepcidin levels and iron metabolism. Constitutive or macrophage-specific expression of a gain-of-function Piezo1 allele in mice causes iron overload, and the E756del allele (present in ~1/3 of individuals of African descent) is strongly associated with increased plasma iron. |
Constitutive and macrophage-specific conditional knock-in of GOF Piezo1 allele in mice, hepcidin measurement, erythrocyte turnover assays, human genetic association in African Americans |
Cell |
High |
33571427
|
| 2022 |
Cryo-EM of PIEZO1 reconstituted in liposome vesicles revealed curved (resting) and flattened (activated) structural states. Membrane tension induces flattening of the blade (~300 nm2 in-plane area expansion), bending of the beam, and detaching/rotating of the cap, collectively gating the ion-conducting pathway. The calculated half-maximal activation tension (~1.9 pN/nm) matches experimental values. |
Cryo-EM structural determination of Piezo1 in liposomes, in-plane area and stiffness calculations, comparison with detergent-solubilized structures |
Nature |
High |
35388220
|
| 2022 |
Lipid peroxidation during ferroptosis increases plasma membrane tension, activating Piezo1 and TRP channels, causing cation permeability (Na+/Ca2+ influx, K+ efflux). Piezo1 deletion reduces these cation permeability changes. Oxidized lipids also depress Na+/K+-ATPase activity, and preventing cation content changes attenuates ferroptosis. |
Piezo1 deletion, calcium/sodium/potassium flux measurements, ruthenium red/2-APB channel blockers, ferroptosis induction (GPX4 inhibition), membrane tension measurement |
Current Biology |
High |
36898371
|
| 2022 |
Astrocytic Piezo1 mediates mechanically evoked Ca2+ responses and ATP release (mechano-chemo transduction). Piezo1 deletion in astrocytes severely impairs adult hippocampal neurogenesis and abolishes ATP-dependent potentiation of neural stem cell proliferation. Overexpression of Piezo1 in astrocytes enhances LTP and learning/memory performance. |
Astrocyte-specific conditional knockout, in vivo neurogenesis assays, hippocampal LTP recordings, behavioral tests, ATP release measurement, Piezo1 overexpression |
Neuron |
High |
35963237
|
| 2022 |
PECAM1 interacts with PIEZO1 and directs it to endothelial cell-cell junctions. PECAM1 extracellular N-terminus is critical for this interaction; CDH5 also drives PIEZO1 to junctions but its interaction is dynamic and increases with shear stress. PIEZO1 does not interact with VEGFR2. PIEZO1 is required for Ca2+-dependent formation of adherens junctions and associated cytoskeleton. |
Non-disruptive tagging of native PIEZO1 in mice, reconstitution experiments, high-resolution co-localization microscopy, co-immunoprecipitation, shear stress experiments, adherens junction assays |
Communications Biology |
High |
37005489
|
| 2022 |
Endothelial PIEZO1 mediates leukocyte diapedesis: leukocyte-induced clustering of ICAM-1 synergizes with fluid shear stress to increase endothelial membrane tension and activate PIEZO1, elevating [Ca2+]i and driving phosphorylation of SRC, PYK2, and myosin light chain, opening the endothelial barrier. Endothelium-specific Piezo1 deficiency reduces leukocyte extravasation in vivo. |
Endothelial-specific conditional knockout mice, Ca2+ imaging, phospho-SRC/PYK2/MLC measurements, in vivo inflammation models, ICAM-1 clustering assays |
Blood |
High |
35443048
|
| 2022 |
Piezo1 activation by matrix stiffness in macrophages promotes M1 polarization via the YAP signaling axis. Increased matrix stiffness upregulates Piezo1 expression and activates YAP, favoring M1 and suppressing M2 polarization. YAP inhibitor treatment re-polarizes macrophages to M2. |
Polyacrylamide gels of varying stiffness, Piezo1 expression analysis, YAP activation assays, pharmacological YAP inhibition, macrophage polarization markers, in vivo implant model |
Cell Proliferation |
Medium |
38556840
|
| 2022 |
Piezo1 activation in renal proximal tubular cells by mechanical stretch, compression, or matrix stiffness causes calcium influx, activates calpain2, cleaves talin1, and upregulates integrin β1, driving profibrotic responses. TGF-β1 also upregulates Piezo1 expression to drive profibrotic changes via this pathway. |
HK2 cells and primary mouse proximal tubular cells under mechanical stimulation, Yoda1 pharmacology, Piezo1 siRNA/inhibitor, calpain2 activity assay, talin1 cleavage by western blot, integrin β1 assay, UUO/folic acid mouse models with GsMTx4 treatment |
JCI Insight |
High |
35230979
|
| 2022 |
Piezo1 activation promotes Yap/Taz nuclear localization in periosteal stem cells, which in turn increases β-catenin nuclear localization. YAP directly interacts with β-catenin in the nucleus forming a transcriptional YAP/β-catenin complex that upregulates osteogenic, chondrogenic, and angiogenic factors including VEGF-A. |
Piezo1 agonist Yoda1 treatment of periosteal stem cells, YAP nuclear localization imaging, co-immunoprecipitation of YAP and β-catenin, gene expression assays, conditional knockout mice, fracture healing mouse model |
International Journal of Biological Sciences |
Medium |
35844802
|
| 2023 |
Direct nanoscopic fluorescence imaging of PIEZO1 in living cells revealed that blades are significantly expanded at rest by plasma membrane bending stress, more so than predicted from detergent-solubilized structures. Blade expansion correlates with channel activation, and blade flexibility varies along its length due to decreased inter-subdomain binding strength. |
Single-molecule nanoscopic fluorescence imaging (dSTORM/PAINT) of endogenously tagged PIEZO1 in live cells, chemical and mechanical modulators of channel activity |
Nature |
High |
37587339
|
| 2023 |
Piezo1 provides the mechanistic link between mechanical signals and EGFR-ERK activation. Piezo1 activation triggers clathrin-mediated EGFR endocytosis and ERK activation via Src-p38 kinase-dependent serine phosphorylation of EGFR (not canonical EGF-induced tyrosine autophosphorylation). This Piezo1-dependent pathway promotes nuclear ERK, AP-1 (FOS/JUN), and YAP accumulation. |
Piezo1 agonist/antagonist pharmacology, EGFR endocytosis assays, phosphorylation site analysis (serine vs tyrosine), Src and p38 inhibitors, nuclear ERK/AP-1/YAP imaging, ex vivo lung slice experiments |
Science Advances |
Medium |
37756411
|
| 2023 |
Membrane stretch (detected by AFM with FEM modeling) is the mechanism of PIEZO1 gating in chondrocytes. PIEZO1 drives Ca2+ signaling independently at the highest strains, and factors increasing apparent membrane tension (hypoosmotic prestrain, high compression, low deformation rates) increase PIEZO1-driven Ca2+ signaling. The threshold membrane stretch ratio for PIEZO1 activation is λ=1.9. |
Single-cell AFM compression, finite element modeling, calcium imaging, PIEZO1/2 knockout chondrocytes, hypoosmotic treatment, pharmacological channel blockers |
PNAS |
High |
37459546
|
| 2023 |
PIEZO1 activation in lymphatic endothelial cells by fluid flow causes rapid exocytosis of ANGPT2, ectodomain shedding of TIE1 by ADAM17, and increased TIE/PI3K/AKT signaling, followed by nuclear export of the transcription factor FOXO1, establishing a functional molecular network linking PIEZO1 mechanosensing to transcriptional regulation in lymphatic vessels. |
Piezo1 activation/inhibition in cultured LECs, ANGPT2 exocytosis assays, TIE1 shedding assays (ADAM17 involvement), PI3K/AKT/FOXO1 signaling analysis, conditional knockout mice |
Journal of Clinical Investigation |
High |
38747287
|
| 2023 |
Piezo1 activation in neutrophils during trans-endothelial migration generates spike-like Ca2+ signals, upregulates NADPH oxidase 4 (NOX4), and enhances bactericidal function. PMN-specific Piezo1 deletion impairs bacterial clearance in vivo. Mechanical forces in microfluidic systems recapitulate Piezo1-dependent NOX4 upregulation and bactericidal activation. |
Piezo1-specific conditional knockout in PMNs, intravital imaging, calcium imaging, microfluidic systems, NOX4 expression assays, in vivo bacterial infection models, adoptive transfer experiments |
Immunity |
High |
38091995
|
| 2023 |
Piezo1 channels in brain capillary endothelial cells function as mechanosensors: activation by mechanical forces evokes Ca2+ signals in capillary endothelial cells, and these currents are absent upon endothelial cell-specific Piezo1 deletion. |
Electrophysiology of brain cortical and retinal capillaries, endothelial-specific Piezo1 deletion, genetically encoded Ca2+ indicator mice, ex vivo pressurized retina preparation |
Circulation Research |
High |
35382561
|
| 2023 |
Piezo1 activation increases intracellular Ca2+ in shear-stressed neutrophils, mediating calpain activity and cytoskeleton remodeling, which consequently induces NETosis. Shear-stress-induced NETosis is dependent on Piezo1 expression and is enhanced by NETosis-inducing agents. |
Microfluidics shear stress application, Piezo1 knockdown/overexpression, calcium imaging, calpain activity assays, cytoskeleton imaging, NET quantification |
Nature Communications |
Medium |
39174529
|
| 2023 |
Piezo1 in gastric X/A-like cells senses gastric distention and inhibits ghrelin production through the CaMKKII/CaMKIV-mTOR signaling pathway. X/A-like cell-specific Piezo1 knockout causes hyperghrelinemia, hyperphagia, and susceptibility to overweight; Piezo1 activation by Yoda1 or gastric bead implantation inhibits ghrelin production and decreases food intake. |
X/A-like cell-specific conditional Piezo1 knockout, Yoda1 pharmacology, gastric bead implantation, ghrelin measurements, CaMKKII/CaMKIV/mTOR pathway analysis in mHypoE-42 cell line |
Nature Metabolism |
High |
38467889
|
| 2024 |
PIEZO1 activation in red blood cells triggers Ca2+ influx through PIEZO1, which activates TMEM16F (the long-sought-after RBC phosphatidylserine scramblase). PIEZO1-TMEM16F functional coupling is enhanced in hereditary xerocytosis RBCs with PIEZO1 gain-of-function mutations, leading to increased PS exposure. GsMTx-4 and benzbromarone inhibit PIEZO1 and prevent force-induced PS exposure and hemolysis. |
Calcium influx assays, PS exposure assays, TMEM16F functional coupling in normal and HX patient RBCs, pharmacological inhibition with GsMTx-4 and benzbromarone, echinocytosis/hemolysis assays |
Blood |
High |
38033286
|
| 2024 |
PIEZO1 in cytotoxic T cells upregulates the transcription factor GRHL3, which induces expression of the E3 ubiquitin ligase RNF114. RNF114 binds to filamentous actin causing its downregulation and rearrangement, depressing traction forces in T cells. Blocking PIEZO1 strengthens traction forces and augments cytotoxicity against tumor cells. |
PIEZO1 knockout/antagonist treatment of cytotoxic T cells, traction force microscopy, GRHL3/RNF114 expression analysis, F-actin imaging, tumor killing assays, in vivo tumor model with adoptive T cell transfer |
Nature Biomedical Engineering |
High |
38514773
|
| 2024 |
Macrophage Piezo1 promotes progression of liver fibrosis by activating the Ca2+-dependent calpain protease, which drives CTSS (cathepsin S) secretion via cleavage of lysosome-associated membrane protein-1 (LAMP1). Myeloid-specific Piezo1 knockout reduces macrophage inflammation, CTSS secretion, and liver fibrosis. |
Myeloid-specific conditional Piezo1 knockout mice, RNA-seq, CTSS activity assays, calpain inhibition, LAMP1 cleavage western blot, liver fibrosis models (CCl4/BDL) |
Theranostics |
Medium |
37908726
|
| 2024 |
Piezo1 in ILC2s restrains group 2 innate lymphoid cell-driven type 2 lung inflammation. Yoda1 inhibits ILC2 cytokine secretion and proliferation in a KLF2-dependent manner by reducing ILC2 oxidative metabolism. Genetic ablation of Piezo1 in ILC2s exacerbates airway hyperreactivity. |
ILC2-specific conditional Piezo1 knockout mice, Yoda1 pharmacology, cytokine secretion assays, proliferation assays, KLF2 knockdown, metabolic assays (oxidative phosphorylation), in vivo AHR models, humanized mouse models |
Journal of Experimental Medicine |
High |
38530239
|
| 2024 |
Disturbed flow activates Piezo1 in endothelial cells, causing Ca2+ influx that activates the CaM/CaMKII pathway, which phosphorylates FAK and Src, activating YAP and triggering endothelial inflammation. GsMTx4 inhibition of Piezo1 delays atherosclerotic plaque progression. |
Oscillatory shear stress application, Ca2+ imaging, pharmacological inhibition (GsMTx4, CaMKII inhibitor), FAK/Src/YAP phosphorylation assays, ApoE-/- atherosclerosis mouse model |
Journal of the American Heart Association |
Medium |
39450718
|
| 2024 |
Macrophage Piezo1 activation promotes efferocytosis on rigid substrates and facilitates efficient acidification of engulfed cargo in phagolysosomes, driving anti-inflammatory gene expression after efferocytosis. Macrophage-specific Piezo1 knockout impairs efferocytosis and spontaneous resolution of early liver fibrosis. |
Macrophage-specific conditional Piezo1 knockout, polyacrylamide gel stiffness assays, phagolysosomal acidification assays, anti-inflammatory gene expression, in vivo liver fibrosis resolution model, Yoda1 pharmacology |
Science Advances |
Medium |
38838160
|
| 2024 |
Piezo1 in podocytes triggers a signaling loop involving NFATc1 and TRPC6, leading to increased calcium influx and perpetuating podocyte injury in diabetic kidney disease. TRPC6 overexpression in podocyte-specific Piezo1 knockout mice counteracted the protective effects of Piezo1 deletion, confirming the Piezo1/NFATc1/TRPC6 axis. |
Podocyte-specific Piezo1 conditional knockout mice, DKD model (STZ+HFD), in vitro calcium influx assays, NFATc1 and TRPC6 expression analysis, AAV-mediated TRPC6 overexpression rescue experiment |
JASN |
Medium |
39932793
|
| 2025 |
Piezo1 in pulmonary myofibroblasts (periostin+ cells) mediates mechanosensation essential for myofibroblast activation and lung fibrosis. Loss of Piezo1 in periostin+ cells disrupts actin organization and prevents Yap/Taz nuclear localization, shifting myofibroblasts from a proliferative to an apoptotic state. Myofibroblast-specific Yap/Taz deletion fully recapitulates protective Piezo1-KO phenotypes. |
Postn-specific conditional Piezo1 knockout mice, actin organization imaging, Yap/Taz nuclear localization assays, myofibroblast-specific Yap/Taz knockout for epistasis, bleomycin pulmonary fibrosis model |
Journal of Clinical Investigation |
High |
40454481
|
| 2025 |
PIEZO1 in vascular smooth muscle cells attenuates Marfan syndrome aortic aneurysm by inhibiting the TGF-β signaling pathway through promoting endocytosis and autophagy of TGF-β receptor 2 (TGFBR2) via Rab GTPase 3C. Smooth muscle cell-specific Piezo1 knockout exacerbates aneurysm and TGF-β pathway activation; Yoda1 activation reverses aneurysm development. |
VSMC-specific conditional Piezo1 knockout in MFS mice, TGFBR2 endocytosis and autophagy assays, Rab3C involvement, Yoda1 pharmacological treatment in vivo, TGF-β pathway signaling assays |
European Heart Journal |
Medium |
39585648
|
| 2025 |
Piezo1 in cardiomyocytes is elevated in diabetic cardiomyopathy and promotes mitochondrial fission via calpain activation and Drp1 dephosphorylation. Cardiac-specific Piezo1 knockout restores ERK1/2-mediated Drp1 phosphorylation (inhibitory), preserves mitochondrial dynamics, and ameliorates diabetic cardiac dysfunction and fibrosis. |
Cardiac-specific conditional Piezo1 knockout mice (STZ and HFD+STZ models), echocardiography, calpain activity assays, Drp1/ERK phosphorylation western blots, mitochondrial morphology and respiration assays, H9C2 cells and neonatal cardiomyocytes |
Cardiovascular Diabetology |
Medium |
40114130
|
| 2022 |
Piezo1 activation stimulates mitochondrial calcium uptake and oxidative phosphorylation (OXPHOS). Loss of Piezo1 reduces mitochondrial oxygen consumption rate and ATP production in calvarial cells, associated with increased phosphodiesterase Pde4a expression and lower cAMP levels. cAMP signaling via PKA is required for the Piezo1-induced increase in mitochondrial OXPHOS. |
Piezo1 conditional knockout and agonist treatment in calvarial cells, Seahorse OCR measurements, cAMP reporter assays, phosphodiesterase inhibition, PKA inhibition, mitochondrial calcium imaging |
FASEB Journal |
Medium |
36052712
|
| 2022 |
Piezo1 in lymphatic endothelial cells acts as the upstream mechanosensor for flow-induced Orai1-KLF2-Notch lymphatic mechanotransduction pathway. Piezo1 knockdown blocks laminar flow-induced calcium influx and Orai1 downstream gene regulation; Piezo1 stimulation activates Orai1 signaling without fluid flow; Orai1 inhibition blocks Piezo1-mediated mechanotransduction, establishing Piezo1 epistatic to Orai1. |
Lymphatic endothelial cell Piezo1 knockdown, flow-induced calcium imaging, lymphatic-specific conditional Piezo1 knockout mice, Orai1 inhibition for epistasis, in vivo lymphatic regeneration model, Yoda1 pharmacology for lymphedema treatment |
Circulation Research |
High |
35701867
|