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.
Zou et al. (2025) studied this question.