Mitochondrial mechanisms in septic cardiomyopathy

Abstract

Background Sepsis is the abnormal immune and inflammatory response to infection that may ultimately result in multi-organ failure. Lacking of effective therapy, sepsis and septic shock remain as leading causes of death, especially in patients that sepsis led to severe myocardial dysfunction. However, the mechanisms underlying myocardial injury following sepsis are not clear. Objective This review discusses that sepsis may cause cardiomyopathy through damaging mitochondrial function. Content The major manifestations of septic cardiomyopathy include right and left ventricular pump failure. In sepsis, many substances, including toxins, cytokines, reactive oxygen species, and nitric oxide, are released, and subsequently mobilize a series of pathological procedures, such as, calcium overload, mitochondrial dysfunction, autophage, and apoptosis. Mitochondrial dysfunction and energy depletion likely contribute to septic cardiomyopathy. Trend Early diagnosis of myocardial dysfunction and restoration of normal mitochondrial function may be an effective strategy in the treatment of sepsis and septic shock. Key words: Sepsis; Cardiomyopathy; Mitochondrial dysfunction