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固醇载体蛋白2:动脉粥样硬化发病机制中的一个有前景的靶点。

Sterol carrier protein 2: A promising target in the pathogenesis of atherosclerosis.

作者信息

Xu Can, Li Heng, Tang Chao-Ke

机构信息

Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, The First Affiliated Hospital of University of South China, Department of Cardiology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.

出版信息

Genes Dis. 2022 Jan 10;10(2):457-467. doi: 10.1016/j.gendis.2021.12.007. eCollection 2023 Mar.

DOI:10.1016/j.gendis.2021.12.007
PMID:37223526
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10201558/
Abstract

Atherosclerosis, the underlying pathophysiological basis of cardiovascular disease, has been recognized as a lipid-driven chronic inflammatory disease. Sterol carrier protein 2 (SCP-2) is a 13-kDa non-specific lipid-transfer protein expressed by various tissues and cells, such as liver, heart, vascular smooth muscle cells (VSMCs), and macrophages. SCP-2 has an extensive role in cardiovascular and metabolic diseases. Recently, SCP-2 was reported to promote the development of atherosclerosis by regulating lipid metabolism and peroxidation, endocannabinoid metabolism, vascular inflammation, and fatty acid metabolism. In this review, we summarized the recent advances regarding the role of SCP-2 in the pathogenesis of atherosclerosis and tried to provide a rationale for future investigation and a better understanding of the biological functions of SCP-2 in atherosclerotic cardiovascular disease.

摘要

动脉粥样硬化是心血管疾病的潜在病理生理基础,已被公认为是一种脂质驱动的慢性炎症性疾病。固醇载体蛋白2(SCP-2)是一种由多种组织和细胞表达的13 kDa非特异性脂质转运蛋白,这些组织和细胞包括肝脏、心脏、血管平滑肌细胞(VSMC)和巨噬细胞。SCP-2在心血管和代谢疾病中具有广泛作用。最近,有报道称SCP-2通过调节脂质代谢和过氧化、内源性大麻素代谢、血管炎症和脂肪酸代谢来促进动脉粥样硬化的发展。在本综述中,我们总结了SCP-2在动脉粥样硬化发病机制中的作用的最新进展,并试图为未来的研究提供理论依据,以便更好地理解SCP-2在动脉粥样硬化性心血管疾病中的生物学功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8ea/10201558/32baa4fd3737/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8ea/10201558/d1fa78afcbc7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8ea/10201558/32baa4fd3737/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8ea/10201558/d1fa78afcbc7/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8ea/10201558/32baa4fd3737/gr2.jpg

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Prog Lipid Res. 2021 Jul;83:101109. doi: 10.1016/j.plipres.2021.101109. Epub 2021 Jun 11.
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Leptin in Atherosclerosis: Focus on Macrophages, Endothelial and Smooth Muscle Cells.瘦素在动脉粥样硬化中的作用:聚焦于巨噬细胞、内皮细胞和平滑肌细胞。
Int J Mol Sci. 2021 May 21;22(11):5446. doi: 10.3390/ijms22115446.
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The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis.
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Pharmaceuticals (Basel). 2023 Jun 15;16(6):887. doi: 10.3390/ph16060887.
AIM2 炎性体加剧克隆性造血中的动脉粥样硬化。
Nature. 2021 Apr;592(7853):296-301. doi: 10.1038/s41586-021-03341-5. Epub 2021 Mar 17.
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Pyroptosis is a critical immune-inflammatory response involved in atherosclerosis.细胞焦亡是动脉粥样硬化中涉及的一种关键的免疫炎症反应。
Pharmacol Res. 2021 Mar;165:105447. doi: 10.1016/j.phrs.2021.105447. Epub 2021 Jan 29.
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Estrogen prevent atherosclerosis by attenuating endothelial cell pyroptosis via activation of estrogen receptor α-mediated autophagy.雌激素通过激活雌激素受体α介导的自噬来减轻内皮细胞焦亡,从而预防动脉粥样硬化。
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