Abstract
Despite advances in treatment and care, burn trauma remains the fourth most common type of traumatic injury. Burn-induced cardiac failure is a key factor for patient mortality, especially during the initial post-burn period (the first 24 to 48 h). Mitochondria, among the most important subcellular organelles in cardiomyocytes, are a central player in determining the severity of myocardial damage. Defects in mitochondrial function and structure are involved in pathogenesis of numerous myocardial injuries and cardiovascular diseases. In this article, we comprehensively review the current findings on cardiac mitochondrial pathological changes and summarize burn-impaired mitochondrial respiration capacity and energy supply, induced mitochondrial oxidative stress, and increased cell death. The molecular mechanisms underlying these alterations are discussed, along with the possible influence of other biological variables. We hope this review will provide useful information to explore potential therapeutic approaches that target mitochondria for cardiac protection following burn injury.
Highlights
Despite advances in treatment and care, burn trauma remains the fourth most common type of traumatic injury
Given aGiven growing body of studies on studies burn trauma-induced pathological alterations of alterations mitochondria mitochondria in diverse tissue/organs, we systematically review the current findings on cardiac in diverse tissue/organs, we systematically review the current findings on cardiac mitochondrial mitochondrial pathological changes
We focus on discussing of TNF-α, IL-1β, and IL-6 on cardiac mitochondria given their important roles in regulating the the influence of TNF-α, IL-1β, and IL-6 on cardiac mitochondria given their important roles in pathological response to burn [2,4,50]
Summary
Despite advances in treatment and care, burn trauma remains the fourth most common type of traumatic injury. Of note, impaired cardiovascular function has been noticed as one of the main determinants of acute phase responses of multiple organ dysfunction following severe thermal injury [2]. Cardiac dysfunction is described by slowed isovolumic relaxation, impaired contractility, and decreased diastolic compliance of the left ventricle in animal models [12,13]. This hemodynamic change istobelieved to be constrictionconstriction following thermal injury This hemodynamic change is believed be a primary afactor primary factor resulting in decreased cardiac output at the early stage of burn injury. Substantial substantial hemodynamic hemodynamic and and cardiac cardiac dysfunction dysfunction following following major burn injury contribute to the development of sepsis, multiple organ failure, and death [3]. Major burn injury contribute to the development of sepsis, multiple organ failure, and death [3].
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