Progress in the mechanism of mitochondrial dysfunction in septic cardiomyopathy

Abstract

Sepsis is a common complication after severe trauma, burns, infections, major surgery and is frequently followed by septic shock, multiple organ dysfunction syndrome, and death. Cardiac dysfunction is a non-negligible component of multiple organ dysfunction in sepsis. However, the specific mechanism of septic cardiomyopathy remains unclear. The results showed that in septic cardiomyopathy, there was damage to cardiomyocytes, while cell death was rare. A growing body of research has shown that mitochondria play an essential role in organ damage in sepsis. The severity of mitochondrial dysfunction is closely related to the prognosis of sepsis and cardiac dysfunction. To date, the mechanisms involved in mitochondrial dysfunction in septic cardiomyopathy include mitochondrial oxidative stress, Ca2+ overload, inflammatory pathways, energy deficiency, and mitochondrial dynamics. It is evident that damaged mitochondria in cardiomyocytes can be fatal to the heart. However, the exact molecular mechanism and its potential significance are still not fully understood. Here, this review intends to draw conclusions about the mechanisms associated with mitochondrial dysfunction in septic cardiomyopathy and to delve into the mechanisms involved in order to find new insights into the study of septic cardiomyopathy.