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已发表论文
糖尿病肾病中的程序性细胞死亡：机制与治疗靶向
Authors Tang S, Sun Y, Sun W, Kang X , Zhao X, Jiang L, Gao Q, An X, Ji H, Lian F
Received 10 June 2025
Accepted for publication 5 September 2025
Published 19 September 2025 Volume 2025:18 Pages 13001—13037
DOI https://doi.org/10.2147/JIR.S545938
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Wenjian Li
Shanshan Tang,1,* Yuting Sun,2,* Wenjie Sun,3,4,* Xiaomin Kang,2 Xuefei Zhao,2 Linlin Jiang,2 Qing Gao,2 Xuedong An,2 Hangyu Ji,2 Fengmei Lian2
1College of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, People’s Republic of China; 2Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People’s Republic of China; 3The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, People’s Republic of China; 4Shandong University of Traditional Chinese Medicine, Jinan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Hangyu Ji, Email jihangyuecho@163.com Fengmei Lian, Email lfm565@sohu.com
Abstract: The escalating incidence and mortality of diabetic kidney disease (DKD) underscore the critical need to elucidate its pathogenesis. Programmed cell death (PCD) plays a dual role in maintaining physiological homeostasis and driving pathological processes in DKD. Accumulating evidence demonstrates that apoptosis, autophagy, pyroptosis, and ferroptosis contribute directly or indirectly to DKD progression via distinct gene-regulated signaling pathways. Recently identified PCD modes (eg, necroptosis, parthanatos) remain poorly characterized in DKD, with emerging evidence suggesting crosstalk between different PCD pathways. This review synthesizes current knowledge on PCD-mediated DKD pathogenesis and PCD-targeted therapies, while highlighting research limitations (eg, unclear PCD interactions, translational gaps). We propose that dissecting the multifaceted roles of PCD in DKD will deepen mechanistic understanding and accelerate the development of novel therapeutics, offering significant scientific and clinical benefits.
Keywords: diabetic kidney disease, programmed cell death, apoptosis, autophagy, pyroptosis, ferroptosis
1College of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, People’s Republic of China; 2Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, People’s Republic of China; 3The Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, People’s Republic of China; 4Shandong University of Traditional Chinese Medicine, Jinan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Hangyu Ji, Email jihangyuecho@163.com Fengmei Lian, Email lfm565@sohu.com
Abstract: The escalating incidence and mortality of diabetic kidney disease (DKD) underscore the critical need to elucidate its pathogenesis. Programmed cell death (PCD) plays a dual role in maintaining physiological homeostasis and driving pathological processes in DKD. Accumulating evidence demonstrates that apoptosis, autophagy, pyroptosis, and ferroptosis contribute directly or indirectly to DKD progression via distinct gene-regulated signaling pathways. Recently identified PCD modes (eg, necroptosis, parthanatos) remain poorly characterized in DKD, with emerging evidence suggesting crosstalk between different PCD pathways. This review synthesizes current knowledge on PCD-mediated DKD pathogenesis and PCD-targeted therapies, while highlighting research limitations (eg, unclear PCD interactions, translational gaps). We propose that dissecting the multifaceted roles of PCD in DKD will deepen mechanistic understanding and accelerate the development of novel therapeutics, offering significant scientific and clinical benefits.
Keywords: diabetic kidney disease, programmed cell death, apoptosis, autophagy, pyroptosis, ferroptosis