Sepsis-induced cardiomyopathy (SICM) is a severe condition associated with poor prognosis in sepsis patients, characterized by impaired cardiac function. Mitochondria play a crucial role in energy production, particularly in generating ATP, which is vital for myocardial function. Recent studies indicate that severe sepsis leads to mitochondrial structural abnormalities, such as apoptosis, incomplete autophagy, and mitophagy, and compromises mitochondrial function, resulting in ATP depletion. These mitochondrial dysfunctions contribute significantly to SICM. However, effective treatments remain limited due to the inability of inotropic drugs to function properly in failing myocardium due to excessive inflammatory factors that block β-adrenergic receptors. Mitochondria are central to cardiac energy metabolism and are involved in various cellular processes, including calcium signaling and mitochondrial metabolism. In sepsis, the complex interplay of inflammatory mediators, such as TNF-α, IL-6, and IL-1β, leads to mitochondrial dysfunction, which is associated with multiple organ failure. The pathophysiology of SICM involves mitochondrial structural abnormalities, autophagy and mitophagy, calcium transport, and metabolic disturbances. These abnormalities are linked to cell death mechanisms such as apoptosis, necroptosis, pyroptosis, and ferroptosis. Mitochondrial dysfunction in SICM is also associated with lipid metabolism disorders, where impaired fatty acid transport and oxidation lead to lipid accumulation and lipotoxicity. Additionally, inflammation can trigger pyroptosis and ferroptosis, both of which contribute to cardiac dysfunction. Therapeutic strategies targeting mitochondrial function include antioxidant therapy, metabolic modulation, and regulation of noncoding RNAs. Mitochondria-targeted antioxidants, such as mitoquinone and SS-31, have shown promise in reducing mitochondrial damage and improving cardiac function in septic models. β-adrenergic receptor blockade has also been explored as a potential treatment for SICM, as it can reduce mitochondrial dysfunction and improve cardiac function. Other approaches include activating PGC1α to promote mitochondrial biogenesis and using sirtuin activators to enhance mitochondrial function. Additionally, mitochondrial transplantation has shown potential in restoring mitochondrial function in septic models. In conclusion, mitochondrial dysfunction is a key factor in the pathogenesis of SICM, and targeting mitochondrial function offers promising therapeutic strategies for improving outcomes in sepsis-induced cardiomyopathy. Further research is needed to develop effective treatments that address the complex interplay of mitochondrial dysfunction and sepsis-related pathophysiology.Sepsis-induced cardiomyopathy (SICM) is a severe condition associated with poor prognosis in sepsis patients, characterized by impaired cardiac function. Mitochondria play a crucial role in energy production, particularly in generating ATP, which is vital for myocardial function. Recent studies indicate that severe sepsis leads to mitochondrial structural abnormalities, such as apoptosis, incomplete autophagy, and mitophagy, and compromises mitochondrial function, resulting in ATP depletion. These mitochondrial dysfunctions contribute significantly to SICM. However, effective treatments remain limited due to the inability of inotropic drugs to function properly in failing myocardium due to excessive inflammatory factors that block β-adrenergic receptors. Mitochondria are central to cardiac energy metabolism and are involved in various cellular processes, including calcium signaling and mitochondrial metabolism. In sepsis, the complex interplay of inflammatory mediators, such as TNF-α, IL-6, and IL-1β, leads to mitochondrial dysfunction, which is associated with multiple organ failure. The pathophysiology of SICM involves mitochondrial structural abnormalities, autophagy and mitophagy, calcium transport, and metabolic disturbances. These abnormalities are linked to cell death mechanisms such as apoptosis, necroptosis, pyroptosis, and ferroptosis. Mitochondrial dysfunction in SICM is also associated with lipid metabolism disorders, where impaired fatty acid transport and oxidation lead to lipid accumulation and lipotoxicity. Additionally, inflammation can trigger pyroptosis and ferroptosis, both of which contribute to cardiac dysfunction. Therapeutic strategies targeting mitochondrial function include antioxidant therapy, metabolic modulation, and regulation of noncoding RNAs. Mitochondria-targeted antioxidants, such as mitoquinone and SS-31, have shown promise in reducing mitochondrial damage and improving cardiac function in septic models. β-adrenergic receptor blockade has also been explored as a potential treatment for SICM, as it can reduce mitochondrial dysfunction and improve cardiac function. Other approaches include activating PGC1α to promote mitochondrial biogenesis and using sirtuin activators to enhance mitochondrial function. Additionally, mitochondrial transplantation has shown potential in restoring mitochondrial function in septic models. In conclusion, mitochondrial dysfunction is a key factor in the pathogenesis of SICM, and targeting mitochondrial function offers promising therapeutic strategies for improving outcomes in sepsis-induced cardiomyopathy. Further research is needed to develop effective treatments that address the complex interplay of mitochondrial dysfunction and sepsis-related pathophysiology.