Review

新型降糖药物在糖尿病合并心肌缺血/再灌注损伤中的研究进展

Research progress on the effects of novel hypoglycemic drugs in diabetes combined with myocardial ischemia/reperfusion injury

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AGEING RESEARCH REVIEWS

影响因子:12.4

分区:医学1区 Top / 老年医学1区细胞生物学2区

发表日期:2023 Apr

作者: Tiangui Yang, Daqing Zhang

DOI: 10.1016/j.arr.2023.101884

摘要

急性心肌梗死（AMI）再灌注伴随缺血/再灌注（I/R）损伤，导致心肌梗死面积扩大、梗死心肌愈合不良和左心室重塑不良，从而增加严重不良心血管事件（MACEs）的风险。糖尿病增加心肌对I/R损伤的易感性，降低心肌对心脏保护策略的反应，恶化心肌I/R损伤，并扩大AMI的梗死面积，增加恶性心律失常和心力衰竭的发生率。目前，关于糖尿病合并AMI及I/R损伤的药物干预证据不足。传统降糖药在预防和治疗糖尿病合并I/R损伤中的作用有限。最新证据表明，新型降糖药物可能在预防糖尿病合并心肌I/R损伤方面发挥作用，尤其是胰高血糖素样肽-1受体激动剂（GLP-1 RA）和钠依赖性葡萄糖转运蛋白2抑制剂（SGLT2i），它们可能通过增加冠脉血流、减少急性血栓形成、减轻I/R损伤、降低心肌梗死面积、抑制缺血性心脏的结构和功能重塑、改善心脏功能和减少MACEs的发生，作用机制包括减轻炎症反应、抑制氧化应激和改善血管内皮功能。本文将系统阐述GLP-1 RA和SGLT2i在糖尿病合并心肌I/R损伤中的保护作用及其分子机制，旨在为临床提供参考。

Abstract

Acute myocardial infarction (AMI) reperfusion is associated with ischemia/reperfusion (I/R) injury, which leads to enlarged myocardial infarction size, poor healing of the infarcted myocardium, and poor left ventricular remodeling, thus increasing the risk of major adverse cardiovascular events (MACEs). Diabetes increases myocardial susceptibility to I/R injury, decreases myocardial responsiveness to cardioprotective strategies, exacerbates myocardial I/R injury, and expands the infarct size of AMI, thereby increasing the incidence of malignant arrhythmias and heart failure. Currently, evidence regarding pharmacological interventions for diabetes combined with AMI and I/R injury is lacking. Traditional hypoglycemic drugs have a limited role in the prevention and treatment of diabetes combined with I/R injury. Current evidence suggests that novel hypoglycemic drugs may exert a preventive effect on diabetes combined with myocardial I/R injury, especially glucagon-like peptide-1 receptor agonists (GLP-1 RA) and sodium-dependent glucose transporter protein 2 inhibitors (SGLT2i), which may increase coronary blood flow, reduce acute thrombosis, attenuate I/R injury, decrease myocardial infarction size, inhibit structural and functional remodeling of the ischemic heart, improve cardiac function, and reduce the occurrence of MACEs of diabetes patients combined with AMI via mechanisms such as reduction of inflammatory response, inhibition of oxidative stress, and improvement of vascular endothelial function. This paper will systematically elaborate the protective role and molecular mechanisms of GLP-1 RA and SGLT2i in diabetes combined with myocardial I/R injury, aiming to provide clinical assistance.