Cheng CH, Hao WR, Cheng TH. Targeting neuronal PAS domain protein 2 and KN motif/ankyrin repeat domains 1: Advances in type 2 diabetes therapy. World J Diabetes 2024; 15(11): 2173-2176 [DOI: 10.4239/wjd.v15.i11.2173]
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. Nov 15, 2024; 15(11): 2173-2176 Published online Nov 15, 2024. doi: 10.4239/wjd.v15.i11.2173
Targeting neuronal PAS domain protein 2 and KN motif/ankyrin repeat domains 1: Advances in type 2 diabetes therapy
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-first authors: Chun-Han Cheng and Wen-Rui Hao.
Author contributions: Cheng TH as a co-corresponding author, played a key role in overseeing the revision process, providing critical feedback, and ensuring the editorial's accuracy and coherence; Cheng CH and Hao WR have made substantial contributions, and their equal roles in the preparation of the manuscript are acknowledged. All authors have reviewed and approved the final version of the editorial. Cheng CH and Hao WR are co-first authors and have contributed equally to drafting the Editorial. Their contributions include the initial writing, literature review, and conceptualization of the editorial content.
Conflict-of-interest statement: All authors declare having no conflicts of interest.
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 21, 2024 Revised: August 21, 2024 Accepted: September 13, 2024 Published online: November 15, 2024 Processing time: 86 Days and 22.7 Hours
Abstract
This editorial summarizes the latest literature on the roles of neuronal PAS domain protein 2 and KN motif/ankyrin repeat domain 1 in type 2 diabetes (T2D). We highlight their involvement in β-cell dysfunction, explore their potential as therapeutic targets, and discuss the implications for new treatment strategies. We offer valuable insights into relevant gene regulation and cellular mechanisms relevant for the targeted management of T2D.
Core Tip: This editorial explores the pivotal roles of NPAS2 and KANK1 in type 2 diabetes (T2D). It elucidates their contribution to β-cell dysfunction, highlighting their potential for targeted therapies. Insights from this editorial may guide the development of innovative treatment approaches against T2D.
