Editorial
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Aug 15, 2024; 15(8): 1654-1658
Published online Aug 15, 2024. doi: 10.4239/wjd.v15.i8.1654
Teneligliptin: A potential therapeutic approach for diabetic cardiomyopathy
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, review of literature, writing, and editing the manuscript.
Supported by the Kuwait Foundation for the Advancement of Sciences and Dasman Diabetes Institute, 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 Editor, Research Scientist, Senior Scientist, Department of Genetics and Bioinformatics, Dasman Diabetes Institute, Jassim AlBahar Street, Dasman 15400, Kuwait. ashraf.madhoun@dasmaninstitute.org
Received: March 12, 2024
Revised: May 14, 2024
Accepted: June 12, 2024
Published online: August 15, 2024
Processing time: 135 Days and 19.4 Hours
Core Tip

Core Tip: Zhang et al provided evidence that teneligliptin mitigated diabetic cardiomyopathy. The authors also clarified the undelaying molecular mechanisms, showing that teneligliptin inhibits NADPH oxidase 4, NOD-like receptor protein 3 inflammasome and activates activated protein kinase to maintain myocyte homeostasis. Researchers are encouraged to implement similar studies on humans to delineate the precise mechanism by which teneligliptin influences activated protein kinase and NOD-like receptor protein 3 signaling.