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组蛋白去乙酰化酶的新见解:治疗动脉粥样硬化的潜在治疗靶点。

New Insight in HDACs: Potential Therapeutic Targets for the Treatment of Atherosclerosis.

作者信息

Luan Yi, Liu Hui, Luan Ying, Yang Yang, Yang Jing, Ren Kai-Di

机构信息

Research Center for Clinical System Biology, Translational Medicine Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.

出版信息

Front Pharmacol. 2022 Apr 21;13:863677. doi: 10.3389/fphar.2022.863677. eCollection 2022.

DOI:10.3389/fphar.2022.863677
PMID:35529430
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9068932/
Abstract

Atherosclerosis (AS) features include progressive hardening and reduced elasticity of arteries. AS is the leading cause of morbidity and mortality. An increasing amount of evidence showed that epigenetic modifications on genes serve are a main cause of several diseases, including AS. Histone deacetylases (HDACs) promote the deacetylation at lysine residues, thereby condensing the chromatin structures and further inhibiting the transcription of downstream genes. HDACs widely affect various physiological and pathological processes through transcriptional regulation or deacetylation of other non-histone proteins. In recent years, the role of HDACs in vascular systems has been revealed, and their effects on atherosclerosis have been widely reported. In this review, we discuss the members of HDACs in vascular systems, determine the diverse roles of HDACs in AS, and reveal the effects of HDAC inhibitors on AS progression. We provide new insights into the potential of HDAC inhibitors as drugs for AS treatment.

摘要

动脉粥样硬化(AS)的特征包括动脉逐渐硬化和弹性降低。AS是发病和死亡的主要原因。越来越多的证据表明,基因上的表观遗传修饰是包括AS在内的几种疾病的主要病因。组蛋白脱乙酰酶(HDACs)促进赖氨酸残基的去乙酰化,从而使染色质结构浓缩,并进一步抑制下游基因的转录。HDACs通过转录调控或其他非组蛋白的去乙酰化广泛影响各种生理和病理过程。近年来,HDACs在血管系统中的作用已被揭示,其对动脉粥样硬化的影响也有广泛报道。在本综述中,我们讨论了血管系统中HDACs的成员,确定了HDACs在AS中的不同作用,并揭示了HDAC抑制剂对AS进展的影响。我们为HDAC抑制剂作为AS治疗药物的潜力提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/3a76b4113988/fphar-13-863677-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/0691a10d24dd/fphar-13-863677-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/5289e4631dc6/fphar-13-863677-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/0195ece0877e/fphar-13-863677-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/3a76b4113988/fphar-13-863677-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/0691a10d24dd/fphar-13-863677-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/5289e4631dc6/fphar-13-863677-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/0195ece0877e/fphar-13-863677-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d7e/9068932/3a76b4113988/fphar-13-863677-g004.jpg

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