[Research progress on epigenetics in sepsis-associated acute kidney injury]

Sepsis-associated acute kidney injury (SAKI) is a life-threatening complication of sepsis, whose pathogenesis involves the intricate interplay of multiple factors, including dysregulated host immune-inflammatory responses, microcirculatory disturbances, and metabolic dysfunction. Aberrations in epigenetic modifications, including DNA methylation and histone acetylation, dynamically modulate gene expression networks, thereby influencing cellular metabolic reprogramming, activation of pro-inflammatory signaling pathways, and disruption of microvascular barrier integrity, are closely associated with adverse clinical outcomes in SAKI patients. As a central regulatory hub of gene expression, epigenetic modifications profoundly participate in key pathological processes of SAKI, including immune homeostasis imbalance, metabolic dysregulation, and microcirculatory dysfunction, through remodeling chromatin architecture and non-coding RNA expression profiles. Although emerging evidence suggests that targeting epigenetic regulation may mitigate SAKI-related pathological damage, the precise molecular mechanisms remain incompletely elucidated. This review systematically summarizes the regulatory roles and molecular mechanisms of epigenetic modifications in SAKI, aiming to provide a theoretical foundation for advancing the understanding of SAKI pathogenesis and developing novel therapeutic strategies.