摘要
Hemorrhagic shock (HS) is one of the leading causes of death among young adults worldwide. Multiple organ dysfunction in HS is caused by an imbalance between tissue oxygen supply and demand, which is closely related to the poor prognosis of patient. Mitochondrial dysfunction is one of the key mechanisms contributing to multiple organ dysfunction in HS, while mitochondrial quality control regulates mitochondrial function through a series of processes, including mitochondrial biogenesis, mitochondrial dynamics, mitophagy, mitochondrial-derived vesicles, and mitochondrial protein homeostasis. Modulating mitochondrial quality control can improve organ dysfunction. This review aims to summarize the effects of mitochondrial dysfunction on organ function in HS and discuss the potential mechanisms of mitochondrial quality control, providing insights into the injury mechanisms underlying HS and guiding clinical management.
摘要
Hemorrhagic shock, a life-threatening organ hypoperfusion caused by rapid, massive blood loss, is the leading cause of traumatic death in peacetime and wartime. The vascular endothelial glycocalyx (vEG) plays an important role in maintaining microcirculatory homeostasis. Severe ischemia and hypoxia of hemorrhagic shock can damage the vEG, leading to endothelial dysfunction and exacerbated microcirculatory and organ impairments. Therefore, early prevention and treatment of vEG damage in hemorrhagic shock can improve microcirculation dysfunction, which is of paramount importance for therapeutic efficacies and outcomes. There have been many studies on the prevention and treatment of vEG damage in hemorrhagic shock, but none is based on the management of vEG damage. The authors reviewed the progress on the mechanism and preventive and therapeutic strategies of vEG damage caused by hemorrhagic shock, hoping to provide reference for the further research of hemorrhagic shock-induced vEG damage.