Mitochondrial Dynamics in Diabetes Mellitus and Its Complications: Mechanisms, Pathological Roles, and Therapeutic Implications.
- 1Department of Pharmacology of Chinese Materia Medica, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488, China.
- 2Beijing Research Institute of Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, China.
Abstract
Diabetes mellitus (DM) is a progressive metabolic disorder in which mitochondrial dysfunction is increasingly recognized as a central contributor to metabolic deterioration and diabetic complications. However, whether dysregulated mitochondrial dynamics represents a primary pathogenic driver, an adaptive response, or a consequence of metabolic stress remains incompletely understood. This review summarizes current advances in the molecular mechanisms governing mitochondrial fission, fusion, and mitophagy, with particular emphasis on their coordinated roles in mitochondrial quality control rather than isolated morphological changes. We discuss how disrupted mitochondrial dynamics contributes to pancreatic β-cell dysfunction, insulin resistance, diabetic nephropathy (DN), diabetic cardiomyopathy (DCM), diabetic retinopathy (DR), and diabetic osteoporosis (DOP) through context-dependent regulation of oxidative stress, bioenergetics, inflammation, and endoplasmic reticulum-mitochondria crosstalk. Furthermore, we critically evaluate emerging therapeutic strategies, including metformin, sodium-glucose cotransporter 2 inhibitors, mitochondrial fission inhibitors, and mitochondria-targeted antioxidants, highlighting both their therapeutic potential and current translational challenges. We propose that restoring the physiological equilibrium among mitochondrial fission, fusion, and mitophagy, rather than unidirectionally inhibiting a single pathway, represents a more promising strategy for preventing and treating diabetes and its complications.
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BibTeX
@article{wang2026mitochondrial,
title = {{Mitochondrial Dynamics in Diabetes Mellitus and Its Complications: Mechanisms, Pathological Roles, and Therapeutic Implications.}},
author = {Guohua Wang and Yige Zhao and Gaiting Liu and Yuhang Du and Shuchang Liu and Yang Yang and Sitong Bu and Baosheng Zhao},
journal = {International journal of molecular sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27198451},
url = {https://europepmc.org/article/MED/42883700},
note = {CC BY},
}
RIS
TY - JOUR
TI - Mitochondrial Dynamics in Diabetes Mellitus and Its Complications: Mechanisms, Pathological Roles, and Therapeutic Implications.
AU - Guohua Wang
AU - Yige Zhao
AU - Gaiting Liu
AU - Yuhang Du
AU - Shuchang Liu
AU - Yang Yang
AU - Sitong Bu
AU - Baosheng Zhao
PY - 2026
DA - 2026/09/22
JO - International journal of molecular sciences
DO - 10.3390/ijms27198451
UR - https://europepmc.org/article/MED/42883700
AB - Diabetes mellitus (DM) is a progressive metabolic disorder in which mitochondrial dysfunction is increasingly recognized as a central contributor to metabolic deterioration and diabetic complications. However, whether dysregulated mitochondrial dynamics represents a primary pathogenic driver, an adaptive response, or a consequence of metabolic stress remains incompletely understood. This review summarizes current advances in the molecular mechanisms governing mitochondrial fission, fusion, and mitophagy, with particular emphasis on their coordinated roles in mitochondrial quality control rather than isolated morphological changes. We discuss how disrupted mitochondrial dynamics contributes to pancreatic β-cell dysfunction, insulin resistance, diabetic nephropathy (DN), diabetic cardiomyopathy (DCM), diabetic retinopathy (DR), and diabetic osteoporosis (DOP) through context-dependent regulation of oxidative stress, bioenergetics, inflammation, and endoplasmic reticulum-mitochondria crosstalk. Furthermore, we critically evaluate emerging therapeutic strategies, including metformin, sodium-glucose cotransporter 2 inhibitors, mitochondrial fission inhibitors, and mitochondria-targeted antioxidants, highlighting both their therapeutic potential and current translational challenges. We propose that restoring the physiological equilibrium among mitochondrial fission, fusion, and mitophagy, rather than unidirectionally inhibiting a single pathway, represents a more promising strategy for preventing and treating diabetes and its complications.
SN - 1422-0067
ER -