Ruimin Tan,1,2 Kexin Wen,1,2 Tianyu Zhao,2,3 He Guo,2,4 Xumin Han,2,4 Jiakai Wang,2,4 Chen Ge,2 Quansheng Du2 

1School of Clinical Medical, North China University of Science and Technology, Tangshan, Hebei, People’s Republic of China; 2Critical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China; 3School of Graduate, Hebei North University, Zhangjiakou, Hebei, People’s Republic of China; 4School of Graduate, Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China

Correspondence: Quansheng Du, Critical Care Department, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of China, Email dqs888@126.com

Abstract: Cuproptosis is a form of programmed cell death triggered by the abnormal accumulation of intracellular copper ions, and its mechanism is closely associated with oxidative stress and mitochondrial dysfunction. Recent studies on sepsis have indicated a potential link between copper metabolism disorders and organ injury. Cuproptosis may be involved in the progression of multi-organ dysfunction in sepsis by disrupting immune homeostasis, promoting inflammatory responses, and altering energy metabolism. This review focuses on the potential role of cuproptosis in sepsis-related damage to major organs, including the heart, liver, lung, and kidney, and summarizes current findings regarding its molecular mechanisms. Potential therapeutic strategies, such as copper chelators and mitochondrial protectants, are also discussed. In addition, this review outlines key areas of ongoing debate and highlights future research directions, with the aim of informing further investigation into precision therapies for sepsis.

Keywords: cuproptosis, sepsis, oxidative stress, mitochondrial dysfunction, targeted therapy