Abstract
Sepsis is an infection-induced syndrome driven primarily by dysregulated host inflammatory responses. This process induces complex physiological changes that provoke systemic inflammation and multi-organ dysfunction, severely threatening survival in advanced cases. N6-methyladenosine (m(6)A), the most prevalent eukaryotic RNA modification, orchestrates crucial regulatory functions across biological processes and is a focal point in epigenetics. This modification is dynamically controlled by three protein classes: writers that catalyze m(6)A deposition, erasers that mediate its removal, and readers that decode modification signals. Substantial evidence implicates m(6)A dysregulation in sepsis-induced multi-organ damage, encompassing cardiovascular dysfunction, acute lung injury, and acute kidney injury. This review synthesizes current mechanistic insights into m(6)A's role in sepsis pathogenesis. By delineating how m(6)A governs inflammatory cascades and organ injury pathways, we evaluate its therapeutic targeting potential, providing translational frameworks for future research.