Contribution and Regulation of Forkhead Transcription Factor O1 during the Renal Fibrosis / 中国生物化学与分子生物学报

ABSTRACT

Chronic kidney disease (CKD) has become a chronic disease that cannot be ignored all over the world. Renal fibrosis is the final result and key pathological features of CKD. The whole process of renal fibrosis is associated with the repair and healing of kidney damage, and this long-term chronic stimulation promotes the renal fibrosis to the kidney failure, it is characterized by continuous activation of myofibroblasts and excessive production and deposition of extracellular matrix. Renal fibrosis is a synergistic process mediated by a variety of signaling pathways, and TGF-β / Smad and Wnt / β-catenin signaling pathways are two of the most classic ones. FoxO1 is an important transcription factor in the human body, which is expressed in a variety of cell types and plays an important role in a variety of cell life activities. Current researches have shown that FoxO1 plays an important role in renal fibrosis. FoxO1 regulates the occurrence and development of renal fibrosis through various signaling pathways such as STAT, SIRT1, Wnt / β-catenin, PI-3K / Akt. For example, FoxO1 / STAT regulates TIF and renal tubule apoptosis, SIRT1 / FoxO1 regulates oxidative stress response and lipotoxicity, FoxO1 / β-catenin inhibits the Wnt / β-catenin signaling pathway. In addition, some related studies suggest that FoxO1 / Smad may play a role in renal fibrosis. The contribution and regulation of FoxO1 in the renal fibrosis are reviewed here in order to further clarify the pathogenesis of renal fibrosis, which may bring new clues and prospects for the treatment of CKD.