The Role of Mitochondrial Dysfunction in Sepsis-Associated Acute Kidney Injury: A Narrative Review

Junfei Liu, Jingmin Zheng, Yinghe Xu, Yongpo Jiang Department of Critical Care Medicine, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, 317000, People’s Republic of ChinaCorrespondence: Yinghe Xu, Email [email protected] Yongpo Jiang, Email [email protected]: Sepsis-associated acute kidney injury (SA-AKI) is one of the most frequent complications of sepsis and one of the leading causes of acute kidney injury (AKI), posing a significant threat to patient survival. The pathogenesis of SA-AKI has been linked to mitochondrial dysfunction, according to emerging evidence. Mitochondria serve as the primary energy-producing organelles in cells, and mitochondrial dysfunction can result in insufficient renal energy supply, oxidative stress, and inflammatory responses, all of which can both initiate and exacerbate SA-AKI. Thus, elucidating the role of mitochondrial dysfunction in SA-AKI is of critical importance. Starting from the fundamental mechanisms of mitochondrial dysfunction, this review draws upon more than 130 relevant publications through August 2025, comprehensively summarizes the role of mitochondrial dysfunction in the pathophysiological processes of SA-AKI and the drugs for treating SA-AKI through the improvement of mitochondrial function, while also discussing in detail the potential therapeutic applications of several well-characterized therapeutic targets in SA-AKI, providing important insights into the diagnosis and treatment of this disease. Keywords: sepsis, SA-AKI, mitochondrial dysfunction, therapeutic