ArticleThe Journal of clinical investigation2014
Podocyte-associated talin1 is critical for glomerular filtration barrier maintenance.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 96 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.
- Efficacy and safety of various immunosuppressive agents for pediatric Henoch-Schönlein purpura nephritis (IgA vasculitis nephritis) in Chinese children: a systematic review and network meta-analysis.Frontiers in immunology · 2026Pooled it
- Elevated Piezo levels cause structural and functional alterations inLife science alliance · 2026Article
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- Targeting DPP9 attenuates podocyte injury by regulating NRF2 antioxidant signaling.Frontiers in pharmacology · 2026Article
- Talin1 modulates the Piezo1-YAP axis to regulate endothelial cell inflammation and atherosclerosis.Cellular and molecular life sciences : CMLS · 2025Article
- Patient-specific hiPSC-Podocytes as an in vitro model of genetic FSGS.Scientific reports · 2025Article
- Research Progress on Anti-fibrotic Effects and Mechanisms of Tetrandrine.Chinese journal of integrative medicine · 2025Review
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- IPSC-induced podocytes from a BORS patient with EYA1 gene mutation showed glucocorticoid-resistant and cytoskeletal rearrangement.Cellular and molecular life sciences : CMLS · 2025Article
- Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion.Journal of the American Society of Nephrology : JASN · 2025Article
- Effective calcineurin inhibitor treatment in adult-onset steroid-resistant nephrotic syndrome with a novel splice donor site variant of TRPC6: a case report.CEN case reports · 2025Article
- Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025Review
- Epigallocatechin-3-Gallate Ameliorates Diabetic Kidney Disease by Inhibiting the TXNIP/NLRP3/IL-1β Signaling Pathway.Food science & nutrition · 2024Article
- Roles of myosin 1e and the actin cytoskeleton in kidney functions and familial kidney disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Piezo activity levels need to be tightly regulated to maintain normal morphology and function in pericardial nephrocytes.Scientific reports · 2024Article
- Mechanosensitive Differentiation of Human iPS Cell-Derived Podocytes.Bioengineering (Basel, Switzerland) · 2024Article
- Genetically conditioned interaction among microRNA-155, alpha-klotho, and intra-renal RAS in male rats: Link to CKD progression.Physiological reports · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- Profilin1 is required for prevention of mitotic catastrophe in murine and human glomerular diseases.The Journal of clinical investigation · 2023Article
- Loss of Pinch Proteins Causes Severe Degenerative Disc Disease-Like Lesions in Mice.Aging and disease · 2023Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
Podocytes are specialized actin-rich epithelial cells that line the kidney glomerular filtration barrier. The interface between the podocyte and the glomerular basement membrane requires integrins, and defects in either α3 or β1 integrin, or the α3β1 ligand laminin result in nephrotic syndrome in murine models. The large cytoskeletal protein talin1 is not only pivotal for integrin activation, but also directly links integrins to the actin cytoskeleton. Here, we found that mice lacking talin1 specifically in podocytes display severe proteinuria, foot process effacement, and kidney failure. Loss of talin1 in podocytes caused only a modest reduction in β1 integrin activation, podocyte cell adhesion, and cell spreading; however, the actin cytoskeleton of podocytes was profoundly altered by the loss of talin1. Evaluation of murine models of glomerular injury and patients with nephrotic syndrome revealed that calpain-induced talin1 cleavage in podocytes might promote pathogenesis of nephrotic syndrome. Furthermore, pharmacologic inhibition of calpain activity following glomerular injury substantially reduced talin1 cleavage, albuminuria, and foot process effacement. Collectively, these findings indicate that podocyte talin1 is critical for maintaining the integrity of the glomerular filtration barrier and provide insight into the pathogenesis of nephrotic syndrome.
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Registered trials
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.