Balakumar P. Unleashing the pathological role of epithelial-to-mesenchymal transition in diabetic nephropathy: The intricate connection with multifaceted mechanism. World J Nephrol 2024; 13(2): 95410 [PMID: 38983761 DOI: 10.5527/wjn.v13.i2.95410]
Corresponding Author of This Article
Pitchai Balakumar, PhD, Professor, Director, The Office of Research and Development, Periyar Maniammai Institute of Science & Technology (Deemed to be University), Vallam, Thanjavur 613403, Tamil Nadu, India. pbalakumar2022@gmail.com
Research Domain of This Article
Medicine, Research & Experimental
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Nephrol. Jun 25, 2024; 13(2): 95410 Published online Jun 25, 2024. doi: 10.5527/wjn.v13.i2.95410
Unleashing the pathological role of epithelial-to-mesenchymal transition in diabetic nephropathy: The intricate connection with multifaceted mechanism
Pitchai Balakumar
Pitchai Balakumar, The Office of Research and Development, Periyar Maniammai Institute of Science & Technology (Deemed to be University), Thanjavur 613403, Tamil Nadu, India
Pitchai Balakumar, School of Pharmacy, Faculty of Health and Medical Sciences, Taylor’s University, Subang Jaya 47600, Selangor, Malaysia
Author contributions: Balakumar P collected the literature, conceptualized the study, critically analyzed the literature, wrote the first draft and finalized the manuscript.
Conflict-of-interest statement: The author declares that no competing interests exist.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Pitchai Balakumar, PhD, Professor, Director, The Office of Research and Development, Periyar Maniammai Institute of Science & Technology (Deemed to be University), Vallam, Thanjavur 613403, Tamil Nadu, India. pbalakumar2022@gmail.com
Received: April 9, 2024 Revised: May 17, 2024 Accepted: May 30, 2024 Published online: June 25, 2024 Processing time: 76 Days and 15.9 Hours
Abstract
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.
Core Tip: Measures to maintain epithelial integrity and prevent epithelial-to-mesenchymal transition (EMT) are being investigated as prospective therapeutic options for diabetic nephropathy. Understanding the role of EMT in diabetic nephropathy lays the door for potential therapeutic approaches. The use of transforming growth factor-β inhibitors, renal anti-inflammatory agents, antifibrotics, and antioxidants to target EMT-related pathways and renal fibrosis may have the potential to reduce the evolution of diabetic nephropathy and to prevent kidney damage.
