ArticleJCI insight2022
Steroid-sensitive nephrotic syndrome candidate gene CLVS1 regulates podocyte oxidative stress and endocytosis.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- The Causal Association between Plasma Metabolites-Mediated Immune Cells and Myocardial Infarction: A Mendelian Randomization Study.Arquivos brasileiros de cardiologia · 2026Article
- Whole-genome Sequence Analysis Revealed Novel Subjective Cognitive Decline-associated Genes in 10,763 Chinese.Genomics, proteomics & bioinformatics · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025Review
- Mechanistic Insights Into Redox Damage of the Podocyte in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Modeling metabolic-associated steatohepatitis with human pluripotent stem cell-derived liver organoids.Hepatology communications · 2024Article
- Review
- Oxidative Stress Contributes to Slit Diaphragm Defects Caused by Disruption of Endocytosis.Kidney international reports · 2024Article
- Nutrition for Podocyte Repair in Nephrotic Syndrome?Nutrients · 2023Article
- Engineering antioxidant ceria-zirconia nanomedicines for alleviating podocyte injury in rats with adriamycin-induced nephrotic syndrome.Journal of nanobiotechnology · 2023Article
- Flight for fish in drug discovery: a review of zebrafish-based screening of molecules.Biology letters · 2023Review
- Article
- Collapsing Focal Segmental Glomerulosclerosis in Siblings With Compound Heterozygous Variants inFrontiers in pediatrics · 2022Article
- A New Prognostic Risk Score: Based on the Analysis of Autophagy-Related Genes and Renal Cell Carcinoma.Frontiers in genetics · 2021Article
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
We performed next-generation sequencing in patients with familial steroid-sensitive nephrotic syndrome (SSNS) and identified a homozygous segregating variant (p.H310Y) in the gene encoding clavesin-1 (CLVS1) in a consanguineous family with 3 affected individuals. Knockdown of the clavesin gene in zebrafish (clvs2) produced edema phenotypes due to disruption of podocyte structure and loss of glomerular filtration barrier integrity that could be rescued by WT CLVS1 but not the p.H310Y variant. Analysis of cultured human podocytes with CRISPR/Cas9-mediated CLVS1 knockout or homozygous H310Y knockin revealed deficits in clathrin-mediated endocytosis and increased susceptibility to apoptosis that could be rescued with corticosteroid treatment, mimicking the steroid responsiveness observed in patients with SSNS. The p.H310Y variant also disrupted binding of clavesin-1 to α-tocopherol transfer protein, resulting in increased reactive oxygen species (ROS) accumulation in CLVS1-deficient podocytes. Treatment of CLVS1-knockout or homozygous H310Y-knockin podocytes with pharmacological ROS inhibitors restored viability to control levels. Taken together, these data identify CLVS1 as a candidate gene for SSNS, provide insight into therapeutic effects of corticosteroids on podocyte cellular dynamics, and add to the growing evidence of the importance of endocytosis and oxidative stress regulation to podocyte function.
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