LncRNA NEAT1作为急性心肌梗死合并心律失常的风险标志物及通过miR-624-5p/SAT1调控心肌细胞功能

Abstract

BACKGROUND Arrhythmia is a common complication of acute myocardial infarction (AMI) and can lead to heart failure (HF) in severe cases. PURPOSE This study aims to investigate the diagnostic and prognostic value of lncRNA NEAT1 in AMI complicated by atrial fibrillation (AMI-AF), as well as its effects on cardiomyocyte (AC16) function through the miR-624-5p/SAT1 pathway. METHODS A total of 110 AMI patients without arrhythmia and 130 AMI-AF patients were included in this retrospective study. RT-qPCR was used to detect NEAT1 levels in their serum samples for receiver operating characteristic curve and Kaplan-Meier analyses. Clinical data were collected for correlation, logistic regression, and Cox model analyses. AC16 cells were exposed to OGD/R to simulate AMI pathology in vitro. Commercially available assay kits, RT-qPCR, ELISA and Western blot were utilized to respectively measure ferroptosis markers, ferrous ion levels and fibrosis indicators. RESULTS Serum NEAT1 was upregulated in the AMI-AF cohort, serving as an effective classifier to distinguish AMI from AMI-AF patients and acting as an independent risk factor for predicting AMI-AF occurrence. Compared with AMI-AF patients without subsequent HF, NEAT1 was high-expressed in HF patients and represented an independent predictor of high HF incidence. NEAT1 promoted cardiomyocyte fibrosis by downregulating miR-624-5p and promoted ferroptosis by regulating the miR-624-5p/SAT1 pathway in OGD/R-treated AC16 cells. CONCLUSION NEAT1 serves as a risk marker for AMI-AF occurrence and adverse prognosis. It advanced myocardial fibrosis and ferroptosis processes by modulating miR-624-5p and SAT1, which may represent the pathological molecular mechanism underlying HF development in AMI-AF.