Sepsis-induced cardiomyopathy (SIC) represents a critical complication of sepsis, contributing significantly to morbidity and mortality in septic patients. Emerging evidence underscores the pivotal role of mitochondrial dysfunction in the pathogenesis of SIC. This article provides a comprehensive overview of the intricate interplay between mitochondria and SIC, elucidating the underlying mechanisms and potential therapeutic avenues. Mitochondrial dysfunction in sepsis, characterized by impaired ATP production, oxidative stress, and mitochondrial permeability transition pore opening, contributes to myocardial injury and dysfunction in SIC. Dysregulation of mitochondrial dynamics, biogenesis, and energy metabolism further exacerbates cardiac dysfunction in SIC. Therapeutic strategies targeting mitochondria, including mitochondria-targeted antioxidants and pharmacological agents modulating mitochondrial dynamics and biogenesis, hold promise for preserving cardiac function and improving outcomes in SIC. Continued research efforts aimed at unraveling the molecular pathways involved in mitochondrial dysfunction and exploring novel mitochondria-targeted therapies are essential for advancing our understanding and management of SIC.
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