[Mechanisms of gut-derived trimethylamine-N-oxide in mediating multiple organ injury in post-cardiac arrest syndrome].

Post-cardiac arrest syndrome (PCAS) is characterized by systemic ischemia-reperfusion injury as its central pathological basis and is associated with severe multiple organ dysfunction. In recent years, increasing attention has been directed toward the role of gut microbiota dysbiosis and its metabolites in critically ill conditions. Among these metabolites, gut-derived trimethylamine-N-oxide (TMAO) has emerged as a key mediator involved in the pathophysiological progression of PCAS. TMAO contributes to the development of PCAS at the multi-organ level through multiple mechanisms, including aggravation of myocardial ischemia-reperfusion injury and ventricular remodeling, exacerbation of neurological dysfunction, induction of renal tubular injury and fibrosis, enhancement of platelet reactivity, and promotion of thrombosis. Accumulating evidence suggests that TMAO mediates multiple organ injury following PCAS through activation of inflammatory responses, induction of oxidative stress, promotion of mitochondrial dysfunction, and regulation of fibrosis-related signaling pathways. A comprehensive understanding of the mechanisms underlying gut-derived TMAO in PCAS may not only facilitate evaluation of its clinical value as a prognostic biomarker but also provide novel therapeutic strategies targeting gut microbial metabolism to improve outcomes in patients with PCAS.