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心肌梗死的潜在治疗策略: Toll 样受体的作用。

Potential therapeutic strategies for myocardial infarction: the role of Toll-like receptors.

机构信息

Department of Pharmacology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, Henan, China.

Department of Pharmacology, Mohi-Ud-Din Islamic Medical College, Azad Jammu & Kashmir, Mirpur, 10250, Pakistan.

出版信息

Immunol Res. 2022 Oct;70(5):607-623. doi: 10.1007/s12026-022-09290-z. Epub 2022 May 24.

DOI:10.1007/s12026-022-09290-z
PMID:35608723
Abstract

Myocardial infarction (MI) is a life-threatening condition among patients with cardiovascular diseases. MI increases the risk of stroke and heart failure and is a leading cause of morbidity and mortality worldwide. Several genetic and epigenetic factors contribute to the development of MI, suggesting that further understanding of the pathomechanism of MI might help in the early management and treatment of this disease. Toll-like receptors (TLRs) are well-known members of the pattern recognition receptor (PRR) family and contribute to both adaptive and innate immunity. Collectively, studies suggest that TLRs have a cardioprotective effect. However, prolonged TLR activation in the response to signals generated by damage-associated molecular patterns (DAMPs) results in the release of inflammatory cytokines and contributes to the development and exacerbation of myocardial inflammation, MI, ischemia-reperfusion injury, myocarditis, and heart failure. The objective of this review is to discuss and summarize the association of TLRs with MI, highlighting their therapeutic potential for the development of advanced TLR-targeted therapies for MI.

摘要

心肌梗死(MI)是心血管疾病患者的一种危及生命的病症。MI 会增加中风和心力衰竭的风险,是全球发病率和死亡率的主要原因。一些遗传和表观遗传因素促成了 MI 的发展,这表明进一步了解 MI 的发病机制可能有助于这种疾病的早期管理和治疗。Toll 样受体(TLRs)是模式识别受体(PRR)家族的知名成员,有助于适应性和先天性免疫。总的来说,研究表明 TLRs 具有心脏保护作用。然而,在对损伤相关分子模式(DAMPs)产生的信号的反应中,TLR 的长期激活会导致炎症细胞因子的释放,并导致心肌炎症、MI、缺血再灌注损伤、心肌炎和心力衰竭的发展和恶化。本综述的目的是讨论和总结 TLR 与 MI 的关联,强调它们在开发针对 MI 的先进 TLR 靶向治疗中的治疗潜力。

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Key role of Extracellular RNA in hypoxic stress induced myocardial injury.
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