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Hypoxia induces the overexpression of Hilpda, which leads to triglyceride overload and FAO defects by downregulating adipose triglyceride lipase (ATGL), triggering mitochondrial dysfunction and upregulating profibrotic factors (TGF-1, -SMA, type I collagen) while reducing the expression of cyclin-dependent kinase 1 (CDK1) and increasing the CyclinB1/D1 ratio, collectively promoting renal tubular fibrosis [85]

However, this clear picture becomes complicated when contrasted with environmental exposure studies

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