Role of M6a Methylation in Myocardial Ischemia-Reperfusion Injury and Doxorubicin-Induced Cardiotoxicity.

IF 3.4 3区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Toxicology Pub Date : 2024-09-01 Epub Date: 2024-07-18 DOI:10.1007/s12012-024-09898-7
Yanfang Liu, Hui Wu, Gang Zhou, Dong Zhang, Qingzhuo Yang, Yi Li, Xiaoting Yang, Jianfeng Sun
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Abstract

Cardiovascular disease remains the leading cause of death worldwide, with acute myocardial infarction and anticancer drug-induced cardiotoxicity being the significant factors. The most effective treatment for acute myocardial infarction is rapid restoration of coronary blood flow by thrombolytic therapy or percutaneous coronary intervention. However, myocardial ischemia-reperfusion injury (MI/RI) after reperfusion therapy is common in acute myocardial infarction, thus affecting the prognosis of patients with acute myocardial infarction. There is no effective treatment for MI/RI. Anthracyclines such as Doxorubicin (DOX) have limited clinical use due to their cardiotoxicity, and the mechanism of DOX-induced cardiac injury is complex and not yet fully understood. N6-methyladenosine (m6A) plays a crucial role in many biological processes. Emerging evidence suggests that m6A methylation plays a critical regulatory role in MI/RI and DOX-induced cardiotoxicity (DIC), suggesting that m6A may serve as a novel biomarker and therapeutic target for MI/RI and DIC. M6A methylation may mediate the pathophysiological processes of MI/RI and DIC by regulating cellular autophagy, apoptosis, oxidative stress, and inflammatory response. In this paper, we first focus on the relationship between m6A methylation and MI/RI, then further elucidate that m6A methylation may mediate the pathophysiological process of MI/RI through the regulation of cellular autophagy, apoptosis, oxidative stress, and inflammatory response. Finally, briefly outline the roles played by m6A in DIC, which will provide a new methodology and direction for the research and treatment of MI/RI and DIC.

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M6a 甲基化在心肌缺血再灌注损伤和多柔比星诱导的心脏毒性中的作用
心血管疾病仍然是全球死亡的主要原因,其中急性心肌梗死和抗癌药物引起的心脏毒性是重要因素。急性心肌梗死最有效的治疗方法是通过溶栓疗法或经皮冠状动脉介入治疗迅速恢复冠状动脉血流。然而,再灌注治疗后的心肌缺血再灌注损伤(MI/RI)在急性心肌梗死中很常见,从而影响急性心肌梗死患者的预后。目前尚无有效治疗 MI/RI 的方法。多柔比星(DOX)等蒽环类药物因其心脏毒性而限制了临床应用,而 DOX 诱导心脏损伤的机制十分复杂,尚未完全明了。N6-甲基腺苷(m6A)在许多生物过程中发挥着至关重要的作用。新的证据表明,m6A 甲基化在 MI/RI 和 DOX 诱导的心脏毒性(DIC)中起着关键的调节作用,这表明 m6A 可作为 MI/RI 和 DIC 的新型生物标记物和治疗靶点。M6A 甲基化可能通过调节细胞自噬、细胞凋亡、氧化应激和炎症反应来介导 MI/RI 和 DIC 的病理生理过程。本文首先关注 m6A 甲基化与 MI/RI 的关系,然后进一步阐明 m6A 甲基化可能通过调控细胞自噬、凋亡、氧化应激和炎症反应介导 MI/RI 的病理生理过程。最后,简要概述了 m6A 在 DIC 中的作用,这将为 MI/RI 和 DIC 的研究和治疗提供新的方法和方向。
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来源期刊
Cardiovascular Toxicology
Cardiovascular Toxicology 医学-毒理学
CiteScore
6.60
自引率
3.10%
发文量
61
审稿时长
>12 weeks
期刊介绍: Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and signaling pathways of environmental toxicants on the cardiovascular system. Also covered are the detrimental effects of new cardiovascular drugs, and cardiovascular effects of non-cardiovascular drugs, anti-cancer chemotherapy, and gene therapy. In addition, Cardiovascular Toxicology reports safety and toxicological data on new cardiovascular and non-cardiovascular drugs.
期刊最新文献
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