ArticleJournal of the American Society of Nephrology : JASN2016
Loss of Epithelial Membrane Protein 2 Aggravates Podocyte Injury via Upregulation of Caveolin-1.
Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Glomage: A Multimodal Platform for High-Content Morphological and RNA Profiling of Glomeruli in Zebrafish and Mouse Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Endoplasmic reticulum-mediated organelle crosstalk in kidney disease.Nature reviews. Nephrology · 2025Review
- Advances in focal segmental glomerulosclerosis research: genetic causes to non-coding RNAs.Molecular biology reports · 2025Review
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Modeling Podocyte Ontogeny and Podocytopathies with the Zebrafish.Journal of developmental biology · 2023Review
- Review
- Review
- Epithelial membrane protein 2 governs transepithelial migration of neutrophils into the airspace.The Journal of clinical investigation · 2020Article
- Lipid mediators of insulin signaling in diabetic kidney disease.American journal of physiology. Renal physiology · 2019Review
- Corticosteroid treatment exacerbates nephrotic syndrome in a zebrafish model of magi2a knockout.Kidney international · 2019Article
- Genetic Deletion ofFrontiers in medicine · 2019Article
- Triptolide attenuates proteinuria and podocyte apoptosis via inhibition of NF-κB/GADD45B.Scientific reports · 2018Article
- Mutations in six nephrosis genes delineate a pathogenic pathway amenable to treatment.Nature communications · 2018Article
- The transcription factor Dach1 is essential for podocyte function.Journal of cellular and molecular medicine · 2018Article
- The Role of Glucocorticoid Receptors in Podocytes and Nephrotic Syndrome.Nuclear receptor research · 2018Article
- Advillin acts upstream of phospholipase C ϵ1 in steroid-resistant nephrotic syndrome.The Journal of clinical investigation · 2017Article
- Genetics of childhood steroid-sensitive nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2017Review
- Acute podocyte injury is not a stimulus for podocytes to migrate along the glomerular basement membrane in zebrafish larvae.Scientific reports · 2017Article
- Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?Current diabetes reports · 2017Review
- Minimal change disease and idiopathic FSGS: manifestations of the same disease.Nature reviews. Nephrology · 2016Review
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6 authors.
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Abstract
Nephrotic syndrome is a CKD defined by proteinuria with subsequent hypoalbuminemia, hyperlipidemia, and edema caused by impaired renal glomerular filtration barrier function. We previously identified mutations in epithelial membrane protein 2 (EMP2) as a monogenic cause of this disease. Here, we generated an emp2-knockout zebrafish model using transcription activator-like effector nuclease-based genome editing. We found that loss of emp2 in zebrafish upregulated caveolin-1 (cav1), a major component of caveolae, in embryos and adult mesonephric glomeruli and exacerbated podocyte injury. This phenotype was partially rescued by glucocorticoids. Furthermore, overexpression of cav1 in zebrafish podocytes was sufficient to induce the same phenotype observed in emp2 homozygous mutants, which was also treatable with glucocorticoids. Similarly, knockdown of EMP2 in cultured human podocytes resulted in increased CAV1 expression and decreased podocyte survival in the presence of puromycin aminonucleoside, whereas glucocorticoid treatment ameliorated this phenotype. Taken together, we have established excessive CAV1 as a mediator of the predisposition to podocyte injury because of loss of EMP2, suggesting CAV1 could be a novel therapeutic target in nephrotic syndrome and podocyte injury.
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