ArticleJournal of the American Society of Nephrology : JASN2010
Inhibition of podocyte FAK protects against proteinuria and foot process effacement.
Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 127 citations in OpenAlex.
- IL-15 Links Muscle-Kidney Crosstalk to Preserving Podocyte Mitochondrial Fusion and Attenuating Diabetic Nephropathy.Journal of cachexia, sarcopenia and muscle · 2026Article
- Endothelial cell-released CD93 contributes to podocyte injury in idiopathic nephrotic syndrome.Science translational medicine · 2026Article
- Enhanced WWP2 Exacerbates Podocyte Injury in Lupus Nephritis through Monoubiquitylating H2A at K119.International journal of biological sciences · 2026Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion.Journal of the American Society of Nephrology : JASN · 2025Article
- Roles of myosin 1e and the actin cytoskeleton in kidney functions and familial kidney disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- DOT1L protects against podocyte injury in diabetic kidney disease through phospholipase C-like 1.Cell communication and signaling : CCS · 2024Article
- IGFBP2 induces podocyte apoptosis promoted by mitochondrial damage via integrin α5/FAK in diabetic kidney disease.Apoptosis : an international journal on programmed cell death · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- Pharmacological Blockade of the Adenosine ACells · 2024Article
- The spatially resolved transcriptome signatures of glomeruli in chronic kidney disease.JCI insight · 2024Article
- Article
- CdGAP maintains podocyte function and modulates focal adhesions in a Src kinase-dependent manner.Scientific reports · 2022Article
- Pulmonary surfactants and the respiratory-renal connection in steroid-sensitive nephrotic syndrome of childhood.iScience · 2022Article
- Upregulation of OASIS/CREB3L1 in podocytes contributes to the disturbance of kidney homeostasis.Communications biology · 2022Article
- Rapamycin attenuated podocyte apoptosis via upregulation of nestin in Ang II-induced podocyte injury.Molecular biology reports · 2022Article
- Serum IL-12p40: A novel biomarker for early prediction of minimal change disease relapse following glucocorticoids therapy.Frontiers in medicine · 2022Article
- Development of Biomarkers and Molecular Therapy Based on Inflammatory Genes in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- IGFBP-1 expression is reduced in human type 2 diabetic glomeruli and modulates β1-integrin/FAK signalling in human podocytes.Diabetologia · 2021Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that plays a critical role in cell motility. Movement and retraction of podocyte foot processes, which accompany podocyte injury, suggest focal adhesion disassembly. To understand better the mechanisms by which podocyte foot process effacement leads to proteinuria and kidney failure, we studied the function of FAK in podocytes. In murine models, glomerular injury led to activation of podocyte FAK, followed by proteinuria and foot process effacement. Both podocyte-specific deletion of FAK and pharmacologic inactivation of FAK abrogated the proteinuria and foot process effacement induced by glomerular injury. In vitro, podocytes isolated from conditional FAK knockout mice demonstrated reduced spreading and migration; pharmacologic inactivation of FAK had similar effects on wild-type podocytes. In conclusion, FAK activation regulates podocyte foot process effacement, suggesting that pharmacologic inhibition of this signaling cascade may have therapeutic potential in the setting of glomerular injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.