1. Figure 6 Cholesterol metabolism in obesity-related glomerulopathy
Figure 6 | Cholesterol metabolism in obesity-related glomerulopathy. Cholesterol accumulation can occur as a result of increased cholesterol synthesis mediated by sterol regulatory element-binding protein 2 (SREBP-2) and its target enzymes including 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR); increased cholesterol uptake mediated by LDL receptor, oxidized LDL receptor, scavenger receptor A (SRA) or CD36; decreased cholesterol efflux mediated by liver X receptor (LXR) and target enzymes; or decreased cholesterol catabolism mediated by bile acids and bile acid transporters. LXR agonists increase cholesterol efflux and decrease inflammation and endoplasmic reticulum stress. ABCA1, ATP-binding cassette subfamily A member 1; ABCG1, ATP-binding cassette subfamily G member 1; HMGCR, hydroxymethylglutaryl-CoA reductase kinase.
D’Agati, V. D. et al. (2016) Obesity-related glomerulopathy: clinical and pathologic characteristics and pathogenesis
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