Institute of Cardiovascular Diseases, China Three Gorges University, Hubei, China.
Department of Cardiology, Yichang Central People's Hospital, Yichang, 443003, China.
Cardiovasc Toxicol. 2024 Sep;24(9):918-928. doi: 10.1007/s12012-024-09898-7. Epub 2024 Jul 18.
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.
心血管疾病仍然是全球范围内的主要死亡原因，其中急性心肌梗死和抗癌药物诱导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治疗或经皮冠状动脉介入术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。MI/RI 目前尚无有效治疗方法。阿霉素（DOX）等蒽环类药物由于其心脏毒性，临床应用受到限制，而 DOX 诱导的心脏损伤机制复杂，尚未完全阐明。N6-甲基腺苷（m6A）在许多生物学过程中发挥着至关重要的作用。新出现的证据表明，m6A 甲基化在 MI/RI 和 DOX 诱导的心脏毒性（DIC）中发挥着关键的调节作用，表明 m6A 可能作为 MI/RI 和 DIC 的新型生物标志物和治疗靶点。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。在本文中，我们首先关注 m6A 甲基化与 MI/RI 的关系，然后进一步阐明 m6A 甲基化可能通过调节细胞自噬、细胞凋亡、氧化应激和炎症反应来介导 MI/RI 的病理生理过程。最后，简要概述 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。
