Zou Yuanxia, Dai Jian, Li Jianchun, Liu Min, Li Run, Li Guiping, Lai Junyu, Wang Li
Research Center for Integrated Traditional Chinese and Western Medicine, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
Department of Neurology, The Third People's Hospital of Luzhou, Luzhou, Sichuan 646000, P.R. China.
Int J Mol Med. 2025 Oct;56(4). doi: 10.3892/ijmm.2025.5603. Epub 2025 Aug 1.
The progression from acute kidney injury (AKI) to chronic kidney disease (CKD) has become a focal point of investigation, with the TGF‑β/Smad signaling pathway emerging as a key mediator in this process. The present review assesses how TGF‑β/Smad contributes to renal fibrosis and the subsequent deterioration of kidney function following AKI. Drawing on recent experimental and clinical findings, this study explores how pathway activation promotes tubular cell injury, inflammation and interstitial fibrosis. By examining these molecular and cellular events, this study offers fresh insights into the complex mechanisms that underlie the AKI‑CKD transition and highlights potential therapeutic strategies aimed at interrupting or slowing disease progression.
从急性肾损伤(AKI)发展为慢性肾脏病(CKD)已成为研究的焦点,转化生长因子-β(TGF-β)/Smad信号通路在此过程中成为关键介质。本综述评估了TGF-β/Smad如何导致肾纤维化以及AKI后肾功能的后续恶化。基于最近的实验和临床研究结果,本研究探讨了该信号通路的激活如何促进肾小管细胞损伤、炎症和间质纤维化。通过研究这些分子和细胞事件,本研究为AKI-CKD转化的复杂机制提供了新的见解,并突出了旨在阻断或减缓疾病进展的潜在治疗策略。