Septic cardiomyopathy ( SIC) is an organ dysfunction frequently observed in sepsis and characterized by high mortality and poor prognosis. Understanding the complex pathogenesis of SIC and developing effective therapeutic tools are critical issues that require attention. Previous studies have demonstrated the significant role of mitochondrial dysfunction in the development of SIC. In the presence of SIC, and the mitochondrial dysfunction that result, the aberrant regulation of the mitochondrial quality control system (MQC) can exacerbate cardiomyocyte injury. Recent studies have demonstrated that the MQC maintains the dynamics of mitochondrial homeostasis through its regulation of mitochondrial biogenesis, fusion / fission, and autophagy. This article provides an overview of the role of MQC in SIC pathogenesis,reviews the latest studies in the field, and analyzes MQC’s potential as a therapeutic target.