microRNA‐26a‐5p affects myocardial injury induced by coronary microembolization by modulating HMGA1

Coronary microembolization (CME) occurs when atherosclerotic plaque debris is detached during the treatment of acute coronary syndrome with Percutaneous Coronary Intervention (PCI). The complications of distal microvascular embolism, including local myocardial inflammation, are the main causes of myocardial damage and are a strong predictor of poor long‐term prognosis and major cardiac adverse events. microRNAs (miRNAs) are involved in the pathophysiological processes of cardiovascular inflammatory diseases. Dysregulation of microRNA (miR)‐26a‐5p, in particular, is associated with a variety of cardiovascular diseases. However, the role of miR‐26a‐5p in CME‐induced myocardial injury is unclear. In this study, we developed an animal model of CME by injecting microembolic balls into the left ventricle of rats and found that miR‐26a‐5p expression decreased in myocardial tissue in response. Using a miR‐26a‐5p mimic, echocardiography, hematoxylin‐eosin staining, and Western blot analysis we found that the diminished cardiac function and myocardial inflammation induced by CME is alleviated by miR‐26a‐5p overexpression. Furthermore, our results show that inhibitors of miR‐26a‐5p have the opposite effect. In addition, in vitro experiments using real‐time PCR, Western blot analysis, and a dual luciferase reporter gene show that HMGA1 is a target gene of miR‐26a‐5p. Thus, overexpression of miR‐26a‐5p could be a novel therapy to improve CME‐induced myocardial damage. 1. HMGA1 is a target gene downstream of miR‐26a‐5p and is involved in the process of coronary microembolization (CME)‐induced myocardial inflammation. 2. MiR‐26a‐5p plays a key role in CME‐induced myocardial injury, and its specific molecular mechanism may occur through the regulation of the HMGA1/NF‐κB/TNF‐α pathway. 3. Overexpression of miR‐26a‐5p may be a new treatment for myocardial damage caused by CME.