ArticleInternational journal of molecular sciences2025
Type 2 Diabetes Induces Mitochondrial Dysfunction in Zebrafish Skeletal Muscle Leading to Diabetic Myopathy via the miR-139-5p/NAMPT Pathway.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed.
- Hypoxic Exercise Alleviates Diabetic Skeletal Myopathy in Zebrafish in Association with Hif1a/Foxo3a Signaling and Mitochondrial Quality Control.International journal of molecular sciences · 2026Article
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Interpretable hybrid deep learning features of pectoralis on low-dose chest CT for detecting type 2 diabetes.Frontiers in endocrinology · 2026Article
- Association of glucose metabolism status and paraspinal muscle degeneration with chronic pain after endoscopic lumbar decompression: a multicentre retrospective study.Frontiers in endocrinology · 2026Article
- Resistance Exercise Counteracts Skeletal Muscle Atrophy in T2DM Mice by Upregulating FGF21 and Activating PI3K/Akt Pathway.Biomolecules · 2025Article
- Jiangtang Tiaozhi Formula Relieves HFD-Induced Obesity Related Type 2 Diabetes by Inhibiting the cGAS-STING Pathway.Journal of cellular and molecular medicine · 2025Article
- Nicotinamide phosphoribosyltransferase in NADCell death discovery · 2025Review
- High-Fat Diet-Induced Diabetic Cardiomyopathy in Female Zebrafish: Cardiac Pathology and Functional Decline Mediated by Type 2 Diabetes.Nutrients · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Type 2 diabetes mellitus (T2DM) is a common metabolic disease that is frequently accompanied by multiple complications, including diabetic myopathy, a muscle disorder that is mainly manifested as decreased muscle function and reduced muscle mass. Diabetic myopathy is a relatively common complication among patients with diabetes that is mainly attributed to mitochondrial dysfunction. Therefore, we investigated the mechanisms underlying diabetic myopathy development, focusing on the role of microRNAs (miRs). Zebrafish were fed a high-sugar diet for 8 weeks and immersed in a glucose solution to establish a model of T2DM. Notably, the fish exhibited impaired blood glucose homeostasis, increased lipid accumulation in the skeletal muscles, and decreased insulin levels in the skeletal muscle. Additionally, we observed various symptoms of diabetic myopathy, including a decreased cross-sectional area of skeletal muscle fibers, increased skeletal muscle fibrosis, a significant decline in exercise capacity, and a significant decrease in mitochondrial respiratory function. Mechanistically, bioinformatic analysis combined with various molecular analyses showed that the miR-139-5p/NAMPT pathway was involved in long-term high-glucose-induced mitochondrial dysfunction in the skeletal muscle, leading to diabetic myopathy. Conclusively, this study provides a basis for the development of novel strategies for the prevention and treatment of diabetic myopathy.
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