期刊
CLINICA CHIMICA ACTA
卷 500, 期 -, 页码 81-86出版社
ELSEVIER
DOI: 10.1016/j.cca.2019.09.022
关键词
LDL-C; LDLR; SREBP2; PCSK9; IDOL; Dyslipidemia
资金
- National Nature Science Fund of China [81600291, 81673722, 81670268, 31871169]
- Nature Science Fundation of Hunan province [2018JJ2348, 2018JJ2346]
- Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study [0223-0002-0002000-54]
- Construct Program of the Pharmaceutical Science Key Discipline in Hunan Province
The SREBP2/LDLR pathway is sensitive to cholesterol content in the endoplasmic reticulum (ER), while membrane low-density lipoprotein receptor (LDLR) is influenced by sterol response element binding protein 2 (SREBP2), pro-protein convertase subtilisin/kexin type 9 (PCSK9) and inducible degrader of LDLR (IDOL). LDL-C, one of the risk factors in cardiovascular disease, is cleared through endocytosis recycling of LDLR. Therefore, we propose that a balance between LDLR endocytosis recycling and PCSK9-mediated and IDOL-mediated lysosomal LDLR degradation is responsible for cholesterol homeostasis in the ER. For statins that decrease serum LDL-C levels via cholesterol synthesis inhibition, the mechanism by which the statins increase the membrane LDLR may be regulated by cholesterol homeostasis in the ER.
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