Sepsis-induced cardiomyopathy (SICM) is a severe condition that significantly increases mortality in sepsis patients, with a 30–70% mortality rate, which is 2–3 times higher than non-cardiac sepsis. SICM results from myocardial cell death, which can lead to cardiac dysfunction. Mitochondria play a crucial role in myocardial energy metabolism by producing adenosine triphosphate (ATP). Recent studies indicate that severe sepsis causes mitochondrial structural abnormalities, such as apoptosis, incomplete autophagy, and mitophagy, leading to ATP depletion and contributing to SICM. However, effective treatments remain elusive. Sepsis impairs the effectiveness of inotropic drugs due to excessive inflammatory factors that block β-adrenergic receptors. The article reviews recent knowledge on myocardial cell death in sepsis, focusing on the role of mitochondria in SICM and discussing potential therapies for sepsis-induced myocardial injury. Mitochondrial dysfunction in SICM is associated with various factors, including calcium transport defects, metabolic abnormalities, and cell death mechanisms such as pyroptosis and ferroptosis. Mitochondrial metabolic abnormalities, such as lipid accumulation, also contribute to SICM. Therapeutic strategies for SICM include antioxidant therapy, metabolic modulation of mitochondrial ATP production, and regulation of noncoding RNAs. Additionally, β-adrenergic receptor blockade may be effective in treating SICM. The article also discusses other approaches, such as activating mitochondrial biogenesis and inhibiting ferroptosis, to restore mitochondrial function. Overall, mitochondrial dysfunction is a key factor in SICM, and targeting mitochondrial function may offer promising therapeutic strategies for SICM.Sepsis-induced cardiomyopathy (SICM) is a severe condition that significantly increases mortality in sepsis patients, with a 30–70% mortality rate, which is 2–3 times higher than non-cardiac sepsis. SICM results from myocardial cell death, which can lead to cardiac dysfunction. Mitochondria play a crucial role in myocardial energy metabolism by producing adenosine triphosphate (ATP). Recent studies indicate that severe sepsis causes mitochondrial structural abnormalities, such as apoptosis, incomplete autophagy, and mitophagy, leading to ATP depletion and contributing to SICM. However, effective treatments remain elusive. Sepsis impairs the effectiveness of inotropic drugs due to excessive inflammatory factors that block β-adrenergic receptors. The article reviews recent knowledge on myocardial cell death in sepsis, focusing on the role of mitochondria in SICM and discussing potential therapies for sepsis-induced myocardial injury. Mitochondrial dysfunction in SICM is associated with various factors, including calcium transport defects, metabolic abnormalities, and cell death mechanisms such as pyroptosis and ferroptosis. Mitochondrial metabolic abnormalities, such as lipid accumulation, also contribute to SICM. Therapeutic strategies for SICM include antioxidant therapy, metabolic modulation of mitochondrial ATP production, and regulation of noncoding RNAs. Additionally, β-adrenergic receptor blockade may be effective in treating SICM. The article also discusses other approaches, such as activating mitochondrial biogenesis and inhibiting ferroptosis, to restore mitochondrial function. Overall, mitochondrial dysfunction is a key factor in SICM, and targeting mitochondrial function may offer promising therapeutic strategies for SICM.