Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes

Pu-Hua Zhang^1*Nuo-Nan Li²Xiang Gu¹Chun-Xia Zhou²Zhen-Zhen Jiang¹Xian-Jun Luo²Hong-Wen Zhu¹Xiaoyong Zhu^1*

• ¹Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi Province, China
• ²Jiujiang Clinical Precision Medicine Research Center, jiujiang, China

Diabetes represents a global chronic health issue and has emerged as a crucial risk factor for cardiovascular diseases (CVD). Myocardial fibrosis (MF), which often accompanies diabetes, plays a pivotal role in the progression of cardiac dysfunction and heart failure (HF). Recent research has highlighted mitochondrial oxidative stress (OS) as a fundamental mechanism driving MF in diabetic conditions. Elevated blood glucose levels and metabolic imbalances lead to mitochondrial impairments, which in turn cause an excessive buildup of reactive oxygen species (ROS), culminating in OS. This OS not only inflicts direct damage on myocardial cells but also facilitates the proliferation of myocardial fibroblasts and collagen accumulation through the activation of specific signaling pathways, thus intensifying MF. Furthermore, MF itself intensifies mitochondrial OS, creating a vicious cycle that ultimately impairs myocardial structure and function. Thus, a thorough understanding of the interaction between mitochondrial OS and MF in diabetes is crucial for identifying effective therapeutic targets and enhancing the early diagnosis and intervention strategies for diabetic cardiomyopathy.