The Role of Mitochondrial Dysfunction and Inflammatory Response in the Pathogenesis of Sepsis-Induced Myocardial Injury: A Mechanistic Study

An-Bu Liu,1– 3 Sheng Wang,4 Yue Shen,4 Lei Ma,1 Jun-Fei Zhang1,3 1Department of Emergency Medical, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, People’s Republic of China; 2State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Xinjiang Medical University, Wulumuqi, Xinjiang, People’s Republic of China; 3Ningxia Key Laboratory of Clinical and Pathogenic Microbiology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, People’s Republic of China; 4School of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia, People’s Republic of ChinaCorrespondence: Jun-Fei Zhang, Email [email protected] Lei Ma, Email [email protected]: Sepsis, a severe systemic infection triggered by the invasion of bacterial, viral, fungal, and other pathogens into human tissues, frequently results in substantial damage to the heart, which is one of the primary organs affected. This myocardial injury is strongly linked to poor patient outcomes in sepsis. Recent research has identified key factors such as mitochondrial dysfunction, metabolic disturbances, cell death, and dysregulated inflammatory responses as critical contributors to the pathogenesis of sepsis-induced myocardial injury (SIMI). These mechanisms not only enhance our understanding of SIMI but also offer potential therapeutic targets. The review aims to investigate the pathophysiological mechanisms driving myocardial injury in sepsis, particularly from the perspective of mitochondrial dysfunction. It will examine the complex interactions between inflammatory dysregulation, calcium homeostasis disruption, metabolic reprogramming, and mitochondrial dysfunction in the onset and progression of SIMI. By exploring therapeutic approaches focused on restoring mitochondrial function, this research aims to establish a theoretical framework for interventions targeting SIMI, thereby providing a robust foundation for the development of targeted therapies for SIMI.Keywords: sepsis-induced myocardial injury, SIMI, inflammatory responses, mitochondrial dysfunction, RCD, metabolic reprogramming