微小RNA对糖尿病心肌病氧化应激的调控

Regulation of Oxidative Stress in Diabetic Cardiomyopathy by MicroRNAs

摘要: 糖尿病在全球范围内是最常见的代谢性疾病，随着生活水平提高，患病率逐年增加，能引起诸多并发症，但其定义尚不明确，其中糖尿病心肌病(DCM)是一种严重威胁人类健康的疾病，是糖尿病一种常见的并发症，对心脏和外周血管均造成损伤，其特征是在排除其他心血管疾病，在糖尿病患者中发生心室功能障碍。目前提出几种糖尿病性心肌病的发病机制中，炎症诱导的氧化应激(OS)仍然是发生糖尿病心肌病的主要危险因素之一，它可引起活性氧(ROS)的增加。心肌细胞产生的ROS会对心脏产生不利影响，它不仅能进一步产生ROS，造成恶性循环，而且也会导致线粒体损伤、炎症、心肌肥大和纤维化，最终导致心功能障碍。微小RNA (microRNAs, miRNAs)是一种内源性非编码小RNAs，在DCM发病中起重要作用。本文目的是阐明microRNAs在DCM中参与炎症诱导氧化应激的潜在作用机制。

Abstract: Diabetes is the most prevalent metabolic disorder worldwide, with its incidence increasing year on year as living standards rise. This condition induces multiple systemic complications, though ambiguity persists in its conceptual definition. Of particular clinical significance is diabetic cardiomyopathy (DCM), a frequent cardiovascular complication characterized by myocardial and peripheral vasculature impairment. Distinctively, DCM manifests as primary ventricular dysfunction in diabetic populations following exclusion of conventional cardiovascular pathologies such as ischemic heart disease or hypertensive cardiomyopathy. Current research delineates several pathogenic mechanisms underlying DCM, with inflammation-driven oxidative stress (OS) emerging as a critical pathophysiological driver. OS triggers excessive reactive oxygen species (ROS) accumulation in cardiomyocytes, initiating a self-perpetuating cycle of redox imbalance. ROS overproduction induces mitochondrial dysfunction, exacerbates inflammatory cascades, promotes hypertrophic remodeling and interstitial fibrosis, ultimately culminating in impaired cardiac contractility and diastolic dysfunction. MicroRNAs (miRNAs), endogenously expressed small non-coding RNAs, have emerged as critical epigenetic regulators in DCM pathogenesis. The purpose of this study is to elucidate the potential mechanism by which microRNAs participate in inflammation-induced oxidative stress in DCM.