Epigenetics of mitochondrial and inflammation in cardiac fibrosis

Cardiac fibrosis (CF) is a reactive remodeling process that occurs in response to myocardial injury. It is characterized by the accumulation of extracellular matrix (ECM) proteins in the cardiac interstitium, resulting in thickening of the myocardial wall and impaired cardiac function. This ultimately leads to heart failure. Various heart injuries, including ischemia and infection, can trigger inflammatory reactions in the heart, leading to chronic inflammation and progressive structural damage, which contribute to CF. Inflammation and fibrosis are closely intertwined and play crucial roles in the development of heart failure. The myocardium, being a highly oxidized tissue, requires high energy for continuous blood pumping. Mitochondria, the energy centers of cells, are essential for maintaining optimal heart performance. They also play a significant role in promoting inflammation and responding to pathogenic infections. In this article, we review the pathological mechanisms of mitochondrial-controlled inflammatory response in CF and explore the inflammatory regulatory effects and molecular mechanisms of CF from an epigenetic perspective. We provide a brief introduction to promising molecular regulatory factors that target epigenetics, which may serve as potential mitochondrial targets for CF. Finally, we discuss the potential application of these findings in improving the treatment and prevention of CF.