Cheng CH, Hao WR, Cheng TH. Unveiling mitochondrial mysteries: Exploring novel tRNA variants in type 2 diabetes mellitus. World J Diabetes 2025; 16(1): 98798 [DOI: 10.4239/wjd.v16.i1.98798]
Corresponding Author of This Article
Tzu-Hurng Cheng, PhD, Professor, Department of Biochemistry, School of Medicine, College of Medicine, China Medical University, No. 91 Xueshi Road, North District, Taichung 404328, Taiwan. thcheng@mail.cmu.edu.tw
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 Diabetes. Jan 15, 2025; 16(1): 98798 Published online Jan 15, 2025. doi: 10.4239/wjd.v16.i1.98798
Unveiling mitochondrial mysteries: Exploring novel tRNA variants in type 2 diabetes mellitus
Chun-Han Cheng, Wen-Rui Hao, Tzu-Hurng Cheng
Chun-Han Cheng, Department of Medical Education, Linkou Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan
Wen-Rui Hao, Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, Ministry of Health and Welfare, Taipei Medical University, New Taipei 23561, Taiwan
Wen-Rui Hao, Division of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 11002, Taiwan
Tzu-Hurng Cheng, Department of Biochemistry, School of Medicine, College of Medicine, China Medical University, Taichung 404328, Taiwan
Co-corresponding authors: Wen-Rui Hao and Tzu-Hurng Cheng.
Author contributions: Cheng CH and Hao WR wrote the paper; Cheng TH revised the paper. All authors have read and approved the final manuscript.
Conflict-of-interest statement: All authors declare that they have no competing interests.
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: Tzu-Hurng Cheng, PhD, Professor, Department of Biochemistry, School of Medicine, College of Medicine, China Medical University, No. 91 Xueshi Road, North District, Taichung 404328, Taiwan. thcheng@mail.cmu.edu.tw
Received: July 5, 2024 Revised: October 21, 2024 Accepted: November 8, 2024 Published online: January 15, 2025 Processing time: 147 Days and 7.3 Hours
Abstract
The recent study of Ding et al provides valuable insights into the functional implications of novel mitochondrial tRNATrp and tRNASer(AGY) variants in type 2 diabetes mellitus (T2DM). This editorial explores their findings, highlighting the role of mitochondrial dysfunction in the pathogenesis of T2DM. By examining the molecular mechanisms through which these tRNA variants contribute to disease progression, the study introduces new targets for therapeutic strategies. We discuss the broader implications of these results, emphasizing the importance of understanding mitochondrial genetics in addressing T2DM.
Core Tip: This editorial highlights the groundbreaking findings of Ding et al, who uncovered novel mitochondrial tRNATrp and tRNASer(AGY) variants associated with type 2 diabetes mellitus (T2DM). By elucidating the functional effects of these variants, the study enhances our understanding of mitochondrial dysfunction in diabetes pathogenesis and suggests new therapeutic targets. Their study underscores the critical role of mitochondrial genetics in developing strategies for managing T2DM.
