TGFB1 and chronic kidney disease: In addition, the acute kidney injury-to-chronic kidney disease transition may involve a wide range of mechanisms, including the action of scar-forming myofibroblasts, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of the epigenetic, gene, and protein alterations leading to common final signaling pathways such as TGF-β1, p16, Wnt/β-catenin pathway involved in renal aging35.