Work

Txnip/ PDK4 ‐Mediated Hyperdependence on Fatty‐Acid Oxidation Amplifies Susceptibility of Diabetic Myocardium to Ischemia–Reperfusion Damage

Year: 2026

Type: article

Abstract: BACKGROUND: Undergoing perioperative ischemia-reperfusion injury (I/RI), the prevalence of adverse cardiac events is high due to increased myocardial vulnerability in diabetic patients. However, the specific mechanisms of increased myocardial vulnerability in diabetes are still unknown. OBJECTIVE: To investigate the specific mechanisms underlying increased myocardial vulnerability in diabetes and to explore potential myocardial protective strategies. METHODS: In this study, we repeatedly verified through single-cell sequencing, fluorescence in situ staining, metabonomics, and animal experiments. RESULTS: Here we show for the first time that the cardiomyocyte subtype (C6 cardiomyocyte) is a cardiomyocyte characterized by myocardial contraction, and the reduction of its number and metabolic heterogeneity is the basis of myocardial ischemia-reperfusion injury in diabetes. Among them, TXNIP/PDK4 mediated metabolic reprogramming is an important reason for myocardial vulnerability in diabetes, and through regulating TXNIP/PDK4, we optimize myocardial energy metabolism. It can significantly improve the vulnerability of diabetes myocardium, play a good role in myocardial protection, and has clinical transformation potential.

Source: Journal of Diabetes

DOI: 10.1111/1753-0407.70277