ArticleClinical and experimental nephrology2026
Loss of Arhgap24 alters glomerular ultrastructure in zebrafish model.
Article in Clinical and experimental nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundARHGAP24, a GTPase-activating protein (GAP) for the Rho family small GTPase Rac1, is highly expressed in podocytes and is thought to contribute to maintaining glomerular filtration barrier. Variants in ARHGAP24 have been implicated in human kidney diseases. However, the physiological requirement of ARHGAP24 in podocytes remains unclear. Here, we generated an arhgap24 knockout (KO) zebrafish, a well-established model organism, to investigate the in vivo role of ARHGAP24 in podocytes.
methodsAn arhgap24 KO zebrafish was generated using the CRISPR/Cas9 double-nicking method with paired CRISPR RNAs targeting sequences flanking an arginine residue essential for GAP activity to increase target specificity and minimize off-target effects. Glomerular and podocyte morphology in adult arhgap24-deficient zebrafish was examined by light, immunofluorescence, and electron microscopy.
resultsWe obtained a homozygous arhgap24 KO mutant lacking the catalytic arginine residue. Microscopic observations of the glomerulus in arhgap24-deficient zebrafish revealed widening of podocyte foot processes and glomerular basement membrane structural changes, including thickening, lamellation, spike-like extensions, and small electron-dense granules, which are typical features of glomerular and podocyte injury associated with disrupted glomerular filtration barrier.
conclusionarhgap24 deficiency altered glomerular ultrastructure in zebrafish. This study provides initial evidence for an in vivo role of ARHGAP24 and suggests a potential link to human kidney disease.
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