Editorial
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Orthop. Feb 18, 2024; 15(2): 101-104
Published online Feb 18, 2024. doi: 10.5312/wjo.v15.i2.101
Mitochondrial dysfunction in type 2 diabetes: A neglected path to skeletal muscle atrophy
Jian-Jun Wu, Hui-Min Xian, Da-Wei Yang, Fan Yang
Jian-Jun Wu, Hui-Min Xian, Fan Yang, Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Da-Wei Yang, Department of Orthopedic Surgery, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, Heilongjiang Province, China
Fan Yang, State Key Laboratory of Component-based Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 30000, China
Co-first authors: Jian-Jun Wu and Hui-Min Xian.
Co-corresponding authors: Da-Wei Yang and Fan Yang.
Author contributions: Wu JJ, Xian HM, Yang DW, and Yang F drafted the manuscript; all authors contributed to the critical review of the manuscript, and have read and approved the final manuscript; Wu JJ and Xian HM contributed equally to this work as co-first authors. Yang DW and Yang F contributed equally to this work as co-corresponding authors. The decision to designate Wu JJ and Xian HM as co-first authors as well as Yang DW and Yang F as co-corresponding authors is based on multiple factors. First, this research was conducted as a collaborative endeavor, and the designation of co-first/co-corresponding authorship accurately reflects the distribution of responsibilities and the considerable effort required to complete the paper. This ensures effective communication and management of post-submission matters, thereby enhancing the paper's quality and reliability. Second, the research team comprises individuals with diverse expertise and skills from various fields, and appointing co-authors best represents this diversity. This approach fosters a more comprehensive and profound examination of the research topic, enriching readers' understanding by presenting multiple expert perspectives. Third, Wu JJ and Xian HM as well as Yang DW and Yang F made equally substantial contributions throughout the research process. Designating them as co-first/co-corresponding authors acknowledges their equal involvement, while also honoring the collaborative spirit and teamwork that characterized this study.
Supported by the Foundation of State Key Laboratory of Component-based Chinese Medicine, No. CBCM2023107; National Natural Science Foundation of China, No. 81901853; and Specially Funded Scientific Research Project of the Fourth Affiliated Hospital of Harbin Medical University, No. HYDSYTB202126.
Conflict-of-interest statement: All the authors have no conflict of interest related to the manuscript.
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: Fan Yang, MD, MMed, PhD, Associate Research Scientist, Occupational Physician, Postdoc, Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, No. 246 Xuefu Road, Nangang District, Harbin 150001, Heilongjiang Province, China. yangfana@sina.com
Received: September 21, 2023
Peer-review started: September 21, 2023
First decision: November 28, 2023
Revised: December 1, 2023
Accepted: January 11, 2024
Article in press: January 11, 2024
Published online: February 18, 2024
Abstract

Over the course of several decades, robust research has firmly established the significance of mitochondrial pathology as a central contributor to the onset of skeletal muscle atrophy in individuals with diabetes. However, the specific intricacies governing this process remain elusive. Extensive evidence highlights that individuals with diabetes regularly confront the severe consequences of skeletal muscle degradation. Deciphering the sophisticated mechanisms at the core of this pathology requires a thorough and meticulous exploration into the nuanced factors intricately associated with mitochondrial dysfunction.

Keywords: Mfn-2, Oxidative stress, Mitochondria metabolism, Skeletal muscle atrophy, Diabetes

Core Tip: Type 2 diabetes mellitus (T2DM) poses a substantial global health challenge. Attaining optimal glycemic control is crucial for mitigating complications and mortality associated with T2DM. However, recent research has unveiled a frequently overlooked complication: The progressive atrophy of skeletal muscle. Mitochondria, pivotal for cellular energy production, uphold a delicate equilibrium in their fusion and fission processes. Investigating the interplay between mitochondrial dysfunction and skeletal muscle atrophy in T2DM is imperative for advancing our comprehension of diabetes. Findings from cellular and animal models suggest that targeting mitochondrial dynamics, particularly through the modulation of Mfn-2, holds promise as a therapeutic strategy to counteract muscle atrophy induced by diabetes. This approach underscores a novel intersection in the management of diabetic complications, forging a connection between metabolic control and muscular health.