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聚焦于心血管疾病中 HOX 簇嵌入的反义 lncRNAs(综述)。

Spotlight on HOX cluster‑embedded antisense lncRNAs in cardiovascular diseases (Review).

机构信息

Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.

Department of Cardiology, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550002, P.R. China.

出版信息

Int J Mol Med. 2023 Dec;52(6). doi: 10.3892/ijmm.2023.5317. Epub 2023 Oct 13.

DOI:10.3892/ijmm.2023.5317
PMID:37830159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10599348/
Abstract

Atherosclerosis is a complex and chronic inflammatory disease driven by multiple pathophysiological processes that are responsible for diverse cardiovascular events. Atherosclerotic cardiovascular disease, despite substantial triumphs in primary and secondary prevention, remains a dominant epidemic that impairs human health. Therefore, deciphering the pathogenesis of atherosclerosis will provide a real‑world translational understanding. Homeobox cluster‑embedded antisense long non‑coding RNAs (HOX‑lncRNAs), a nascent class of lncRNA molecules with versatile roles in cancer, can also orchestrate various cell functions in cardiovascular disorders and have thus captured the attention of many researchers. Subsequently, numerous studies have demonstrated the role of HOX‑lncRNAs as potential modulators of atherosclerosis. Nevertheless, given that the understanding of HOX‑lncRNAs in atherosclerosis is only just emerging, ongoing research must be initiated to thoroughly pinpoint such causal roles. The present review aimed to highlight the important contributions of HOX‑lncRNAs to atherosclerosis and other pivotal biological processes related to cardiovascular disease. The review concludes with a discussion of the limitations, outlook, challenges and possible solutions associated with HOX‑lncRNAs in atherosclerosis. Looking forward, this may lead to extraordinary breakthroughs in revealing the molecular underpinnings of HOX‑lncRNAs and may offer a promising yet challenging landscape for robust therapeutic strategies for atherosclerosis and/or associated cardiovascular disorders.

摘要

动脉粥样硬化是一种由多种病理生理过程驱动的复杂和慢性炎症性疾病,这些过程导致了不同的心血管事件。尽管在一级和二级预防方面取得了重大进展,但动脉粥样硬化性心血管疾病仍然是一种主要的流行疾病,损害着人类的健康。因此,解析动脉粥样硬化的发病机制将提供一个真实世界的转化理解。同源盒簇嵌入反义长非编码 RNA(HOX-lncRNA)是一类新兴的 lncRNA 分子,在癌症中具有多种作用,也可以协调心血管疾病中各种细胞的功能,因此引起了许多研究人员的关注。随后,大量研究表明 HOX-lncRNA 作为动脉粥样硬化的潜在调节剂的作用。然而,鉴于对动脉粥样硬化中 HOX-lncRNA 的理解才刚刚开始,必须启动正在进行的研究,以彻底确定这些因果作用。本综述旨在强调 HOX-lncRNA 对动脉粥样硬化及其他与心血管疾病相关的重要生物学过程的重要贡献。本文最后讨论了 HOX-lncRNA 在动脉粥样硬化中的局限性、展望、挑战和可能的解决方案。展望未来,这可能会在揭示 HOX-lncRNA 的分子基础方面取得非凡的突破,并为动脉粥样硬化和/或相关心血管疾病的稳健治疗策略提供一个有希望但具有挑战性的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/70bf306e55ff/IJMM-52-6-05317-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/b31932b8b43f/IJMM-52-6-05317-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/9cf621540a8e/IJMM-52-6-05317-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/70bf306e55ff/IJMM-52-6-05317-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/b31932b8b43f/IJMM-52-6-05317-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/9cf621540a8e/IJMM-52-6-05317-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0b7/10599348/70bf306e55ff/IJMM-52-6-05317-g02.jpg

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3
Long noncoding RNA HOTAIR facilitates pulmonary vascular endothelial cell apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD.
Mechanism of extract improving atherosclerosis by regulating PGC-1α/Sirt3/Epac1 pathway.
提取物通过调节PGC-1α/Sirt3/Epac1通路改善动脉粥样硬化的机制。
Front Pharmacol. 2024 Nov 19;15:1483518. doi: 10.3389/fphar.2024.1483518. eCollection 2024.
长链非编码 RNA HOTAIR 通过 DNMT1 介导的 Bcl-2 启动子高甲基化促进 COPD 肺血管内皮细胞凋亡。
Respir Res. 2022 Dec 17;23(1):356. doi: 10.1186/s12931-022-02234-z.
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LncRNAs , , and and non-hypertensive associated cerebrovascular stroke patients, and its link to clinical characteristics and severity score of the disease.长链非编码核糖核酸、以及与非高血压相关的脑血管中风患者,及其与该疾病临床特征和严重程度评分的关联。 (注:原文表述不太完整规范,翻译出来的内容可能会稍显生硬,但已尽量忠实原文。)
Noncoding RNA Res. 2022 Nov 2;8(1):96-108. doi: 10.1016/j.ncrna.2022.10.004. eCollection 2023 Mar.
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