[Research advances on the role of mitochondrial dysfunction and metabolic reprogramming in sepsis-associated acute kidney injury].

Sepsis-associated acute kidney injury (SA-AKI) is one of the most prevalent complications of sepsis and a leading cause of acute kidney injury. It not only prolongs hospitalization and increases mortality but may also progress to chronic kidney disease, severely compromising patients' quality of life. Recent studies have highlighted the critical roles of mitochondrial dysfunction and metabolic reprogramming in the pathogenesis of SA-AKI. Mitochondria are the central hub of cellular energy metabolism; their impairment not only disrupts energy supply but also induces oxidative stress, inflammatory responses, and various forms of cell death, collectively contributing to the initiation and progression of SA-AKI. Metabolic reprogramming, another key mechanism underlying SA-AKI, alters cellular nutrient utilization patterns and influences cell death decisions. These two pathogenic mechanisms are not independent but form an intricate interactive network that drives the development of SA-AKI. This article reviews the latest research advances on the roles of mitochondrial dysfunction and metabolic reprogramming in SA-AKI and discusses their interactions, with the aim of providing new ideas for clinical intervention targeting the regulation of key pathways for mitochondrial function restoration or metabolic reprogramming.