Why the study?
Mitochondrial injury is perceived as the main culprit for reduced myocardial performance in septic cardiomyopathy, prompting a need to summarize recent experimental and clinical progress and contemporary interventional options.
This review highlights the critical role of mitochondrial injury in the pathogenesis of septic cardiomyopathy and discusses potential targeted therapeutic interventions.
Mitochondrial injury may drive septic cardiomyopathy; leaves open targeted therapies for clinical translation.
BACKGROUND: Sepsis and septic shock are known to prompt multiple organ failure including cardiac contractile dysfunction, which is typically referred to as septic cardiomyopathy. Among various theories postulated for the etiology of septic cardiomyopathy, mitochondrial injury (both morphology and function) in the heart is perceived as the main culprit for reduced myocardial performance and ultimately heart failure in the face of sepsis. METHODS: Over the past decades, ample of experimental and clinical work have appeared, focusing on myocardial mitochondrial changes and related interventions in septic cardiomyopathy. RESULTS AND CONCLUSION: Here we will briefly summarize the recent experimental and clinical progress on myocardial mitochondrial morphology and function in sepsis, and discuss possible underlying mechanisms, as well as the contemporary interventional options.
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Tan et al. (2019) studied this question.
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