Balakumar Pitchai
The Office of Research and Development, Periyar Maniammai Institute of Science & Technology (Deemed to be University), Thanjavur 613403, Tamil Nadu, India.
School of Pharmacy, Faculty of Health and Medical Sciences, Taylor's University, Subang Jaya 47600, Selangor, Malaysia.
World J Nephrol. 2024 Jun 25;13(2):95410. doi: 10.5527/wjn.v13.i2.95410.
Renal epithelial-to-mesenchymal transition (EMT) is a process in which epithelial cells undergo biochemical changes and transform into mesenchymal-like cells, resulting in renal abnormalities, including fibrosis. EMT can cause diabetic nephropathy through triggering kidney fibrosis, inflammation, and functional impairment. The diverse molecular pathways that drive EMT-mediated renal fibrosis are not utterly known. Targeting key signaling pathways involved in EMT may help ameliorate diabetic nephropathy and improve renal function. In such settings, understanding precisely the complicated signaling networks is critical for developing customized therapies to intervene in EMT-mediated diabetic nephropathy.
肾上皮-间充质转化(EMT)是一个上皮细胞发生生化变化并转化为间充质样细胞的过程,会导致包括纤维化在内的肾脏异常。EMT可通过引发肾脏纤维化、炎症和功能损害导致糖尿病肾病。驱动EMT介导的肾纤维化的多种分子途径尚未完全明确。靶向参与EMT的关键信号通路可能有助于改善糖尿病肾病并提高肾功能。在这种情况下,精确了解复杂的信号网络对于开发定制疗法以干预EMT介导的糖尿病肾病至关重要。