ArticleAmerican journal of physiology. Renal physiology2016
Dosage-dependent role of Rac1 in podocyte injury.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Loss of Arhgap24 alters glomerular ultrastructure in zebrafish model.Clinical and experimental nephrology · 2026Article
- Targeting RAC1 might be a potential therapeutic strategy for diabetic kidney disease: a Mendelian randomization study.International urology and nephrology · 2025Article
- Circulating RAC1 contributed to steroid-sensitive nephrotic syndrome: Mendelian randomization, single-cell RNA-sequencing, proteomic, and experimental evidence.Renal failure · 2024Article
- Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.Science advances · 2024Article
- Article
- A zebrafish model of congenital nephrotic syndrome of the Finnish type.Frontiers in cell and developmental biology · 2022Article
- Transgenic fluorescent zebrafish lines that have revolutionized biomedical research.Laboratory animal research · 2021Review
- Review
- tRNA-Derived Fragments in Podocytes with Adriamycin-Induced Injury Reveal the Potential Mechanism of Idiopathic Nephrotic Syndrome.BioMed research international · 2020Article
- The Role of Trio, a Rho Guanine Nucleotide Exchange Factor, in Glomerular Podocytes.International journal of molecular sciences · 2018Article
- Podocyte-actin dynamics in health and disease.Nature reviews. Nephrology · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Activation of small GTPase Rac1 in podocytes is associated with rodent models of kidney injury and familial nephrotic syndrome. Induced Rac1 activation in podocytes in transgenic mice results in rapid transient proteinuria and foot process effacement, but not glomerular sclerosis. Thus it remains an open question whether abnormal activation of Rac1 in podocytes is sufficient to cause permanent podocyte damage. Using a number of transgenic zebrafish models, we showed that moderate elevation of Rac1 activity in podocytes did not impair the glomerular filtration barrier but aggravated metronidazole-induced podocyte injury, while inhibition of Rac1 activity ameliorated metronidazole-induced podocyte injury. Furthermore, a further increase in Rac1 activity in podocytes was sufficient to cause proteinuria and foot process effacement, which resulted in edema and lethality in juvenile zebrafish. We also found that activation of Rac1 in podocytes significantly downregulated the expression of
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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.