Septic cardiomyopathy (SIC) is a frequently observed organ dysfunction in sepsis, 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 resulting mitochondrial dysfunction, aberrant regulation of the mitochondrial quality control system (MQC) can exacerbate cardiomyocyte injury. Recent studies have demonstrated that the mitochondrial quality control system (MQC) maintains mitochondrial dynamic homeostasis through its regulation of mitochondrial biogenesis, fusion/fission, and autophagy. Consequently, this article provides an overview of the role of MQC in SIC pathogenesis, reviews the latest studies, and analyzes its potential as a therapeutic target.