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孤儿 GPR146:实现胆固醇平衡的另一种治疗途径?

Orphan GPR146: an alternative therapeutic pathway to achieve cholesterol homeostasis?

机构信息

Orphan Receptor Pharmacology Laboratory, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia; Molecular Pharmacology Drug Design, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.

Molecular Pharmacology Drug Design, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia.

出版信息

Trends Endocrinol Metab. 2022 Jul;33(7):481-492. doi: 10.1016/j.tem.2022.04.008. Epub 2022 May 10.

Abstract

Atherosclerosis predisposes to myriad cardiovascular complications, including myocardial infarction and stroke. Statins have revolutionised cholesterol management but they do not work for all patients, particularly those with familial hypercholesterolaemia (FH). Genome-wide association studies have linked SNPs at orphan G protein-coupled receptor 146 (GPR146) to human atherosclerosis but how GPR146 influences serum cholesterol homeostasis was only recently described. Gpr146 deletion in mice reduces serum cholesterol and atherosclerotic plaque burden, confirming GPR146 as a potential therapeutic target for managing circulating cholesterol. Critically, this effect was independent of the low-density lipoprotein receptor. While still an orphan, the activation of GPR146 by serum suggests identification of its endogenous ligand is tantalisingly close. Herein, we discuss the evidence for GPR146 inhibition as a treatment for atherosclerosis.

摘要

动脉粥样硬化易导致多种心血管并发症,包括心肌梗死和中风。他汀类药物彻底改变了胆固醇管理,但它们并不适用于所有患者,尤其是家族性高胆固醇血症(FH)患者。全基因组关联研究将孤儿 G 蛋白偶联受体 146(GPR146)的 SNP 与人类动脉粥样硬化联系起来,但 GPR146 如何影响血清胆固醇稳态直到最近才被描述。小鼠中 Gpr146 的缺失可降低血清胆固醇和动脉粥样硬化斑块负担,证实 GPR146 是管理循环胆固醇的潜在治疗靶点。关键的是,这种作用独立于低密度脂蛋白受体。虽然仍然是孤儿,但血清对 GPR146 的激活表明其内源性配体的鉴定已经近在咫尺。在此,我们讨论了抑制 GPR146 作为动脉粥样硬化治疗方法的证据。

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