Ferroptosis in vascular injury of critically ill patients: implications of gut microbiota regulation.

The treatment strategies for vascular injury-related diseases have made certain progress, but acute cardiovascular and cerebrovascular events, ischemia-reperfusion injury, and sepsis-induced vascular leakage still remain major causes of high mortality in critically ill patients. A deeper understanding of the pathogenesis of vascular-related diseases is crucial for developing more effective treatment methods. Ferroptosis, a recently discovered form of regulated cell death (RCD) distinct from apoptosis, necrosis, pyroptosis, and autophagy, has been shown to play a key role in the progression of vascular-related diseases. In particular, in sepsis-induced vascular leakage, inflammation and oxidative stress increase susceptibility to ferroptosis, leading to tissue damage and adverse outcomes. Inhibition of ferroptosis can significantly reduce the adverse outcomes caused by vascular injury, thereby improving the outcome of patients. This paper focuses on analyzing the molecular mechanisms through which ferroptosis influences vascular injury-related diseases, emphasizing its significance in ICU care. Additionally, the paper explores the role of gut microbiota dysbiosis in inducing ferroptosis, offering new insights into the gut-ferroptosis-vascular axis as a potential therapeutic target for critically ill patients. A deeper understanding of these mechanisms can pave the way for more personalized and effective treatments, ultimately improving patient outcomes and reducing mortality in this high-risk population.