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In diabetic conditions, ANGPTL4 is markedly upregulated in podocytes and tubular cells, leading to several pathological changes (Srivastava et al., 2024) used genetically engineered mouse models to demonstrate that deleting ANGPTL4 in podocytes and/or tubular cells can prevent proteinuria, glomerular and interstitial fibrosis, and preserve kidney function in diabetic mice (Srivastava et al., 2024)