Editorial
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Sep 15, 2024; 15(9): 1837-1841
Published online Sep 15, 2024. doi: 10.4239/wjd.v15.i9.1837
MicroRNA-630: A potential guardian against inflammation in diabetic kidney disease
Ashraf Al Madhoun
Ashraf Al Madhoun, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Dasman 15400, Kuwait
Author contributions: Al Madhoun A designed the overall concept, reviewed the literature, and wrote and edited the manuscript.
Supported by the Kuwait Foundation for the Advancement of Sciences and Dasman Diabetes Institute, Kuwait, No. RACB-2021-007.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
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: Ashraf Al Madhoun, PhD, Academic Research, Senior Scientist, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Jassim AlBahar Street, Dasman 15400, Kuwait. ashraf.madhoun@dasmainstitute.org
Received: March 24, 2024
Revised: May 20, 2024
Accepted: June 17, 2024
Published online: September 15, 2024
Processing time: 156 Days and 1.4 Hours
Abstract

In this editorial, we comment on the article by Wu et al published “MicroRNA-630 alleviates inflammatory reactions in rats with diabetic kidney disease by targeting toll-like receptor 4”. Diabetic kidney disease (DKD) stands as a significant complication occurring from diabetes mellitus, which contributes substantially to the morbidity and mortality rates worldwide. Renal tubular epithelial cell da-mage, often accompanied by inflammatory responses and mesenchymal trans-differentiation, plays a pivotal role in the progression of DKD. Despite extensive research, the intricate molecular mechanisms underlying these processes remain to be determined. Wu et al remarkable work identifies microRNA-630 (miR-630) as an emerging potential regulator of cell migration, apoptosis, and autophagy, prompting investigation into its association with DKD pathogenesis. This study endeavors to elucidate the impact of miR-630 on TEC injury and the inflammatory response in DKD rats. The role of miR-630 in human DKD will be of interest for future studies.

Keywords: Diabetic kidney disease; MicroRNA; MicroRNA-630; Toll-like receptor 4; Inflammation

Core Tip: Wu et al identified microRNA-630 as a promising candidate for the management of diabetic kidney disease, exerting its protective effects through the regulation of toll-like receptor 4-mediated inflammatory pathways. Further research elucidating the precise molecular mechanisms underlying microRNA-630’s actions and its therapeutic potential is warranted, with the ultimate goal of developing targeted interventions to alleviate the burden of diabetic kidney disease and improve patient outcomes.