ArticleiScience2025
Reduced nephrin tyrosine phosphorylation impairs podocyte force transmission and accelerates detachment in disease.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
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Authors and funding
10 authors.
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Abstract
Podocytes are specialized kidney cells that form the slit diaphragm (SD), an intercellular filtration barrier against plasma protein loss. The SD is subject to significant mechanical strain which can be amplified in disease, leading to podocyte detachment. One key SD protein that might intercept mechanical strain and transmit adhesion signals is nephrin, although its influence on podocyte force transmission remains uncharacterized. Using immunoblotting and elastic resonator interference stress microscopy (ERISM), we demonstrate that nephrin clustering induces rapid podocyte force transmission and adhesion protein activation (paxillin, FAK, and p130Cas), which require nephrin tyrosine phosphorylation at its three YDxV motifs. Furthermore, using a model of diabetic nephropathy to amplify mechanical stress
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