Abstract
<p indent="0mm">Cholesterol homeostasis plays an important role in maintaining proper cellular and systemic functions. A means for the cell to acquire cholesterol is low-density lipoprotein receptor (LDLR)-mediated uptake of low-density lipoprotein. Dysfunction of LDLR leads to hypercholesterolemia that ultimately contributes to cardiovascular disease such as atherosclerosis. The stability of LDLR protein is regulated by proprotein convertase subtilisin/kexin type 9 and inducible degrader of the LDLR (IDOL). As an E3 ubiquitin ligase, IDOL is subjected to transcriptional regulation by liver X receptor. It can ubiquitylate LDLR and leads to its degradation in the lysosome. IDOL also mediates the degradation of other LDLR family members including very low-density lipoprotein receptor and apolipoprotein E receptor 2, thus regulating apolipoprotein E levels in the brain. This review summarizes the most recent knowledge about IDOL, from the structure, the mechanism on regulating LDLR, to the transcriptional and post-transcriptional regulation of IDOL, as well as its roles in cardiovascular disease and Alzheimer’s disease. These research advances may provide potential therapeutic targets for treating the aforementioned diseases.
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