ArticleJournal of cachexia, sarcopenia and muscle2025
Deubiquitinating Enzymes Regulate Skeletal Muscle Mitochondrial Quality Control and Insulin Sensitivity in Patients With Type 2 Diabetes.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- USP8 promotes the progression of sepsis-induced acute lung injury by interacting with the USP24 to suppress PGC-1α deubiquitination and expression.Redox biology · 2026Article
- USP30 inhibits wound healing in diabetic foot ulcers by promoting TRAF6-induced ferroptosis and angiogenesis inhibition.Journal of diabetes investigation · 2026Article
- Dietary Protein Restriction Ameliorates Cardiac Inflammaging via AMPK-ULK1-Mediated Mitochondrial Quality Control.Aging cell · 2026Article
- BDH1 Mediates Aerobic Exercise-Induced Improvement in Skeletal Muscle Metabolic Remodeling in Type 2 Diabetes Mellitus.Biomolecules · 2026Article
- From homeostasis to pathology, organelle-specific autophagy in skeletal muscle: a PRISMA-ScR scoping review.Frontiers in physiology · 2026Review
- Ubiquitination modifications as central regulators of metabolic dysfunction in type 2 diabetes mellitus.Frontiers in endocrinology · 2026Review
- Association of magnesium depletion score, triglyceride-glucose index, and C-reactive protein-albumin-lymphocyte index with diabetic sarcopenia: a cross-sectional study based on NHANES 2014-2018 data.American journal of translational research · 2026Article
- Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies.Cell death & disease · 2025Review
- Mitochondrial bioenergetics dysfunction in T2DM: linking oxidative stress to insulin resistance.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundActivation of mitochondrial fission and quality control occur early in the onset of insulin resistance in human skeletal muscle. We hypothesized that differences in mitochondrial dynamics, structure and bioenergetics in humans would explain the onset and progression of type 2 diabetes (T2D).
methodsFifty-eight sedentary adults (37 ± 12 years) were enrolled into one of three groups: (1) healthy weight (HW), (2) overweight and obesity (Ow/Ob), or (3) T2D. Body composition, aerobic capacity, and insulin sensitivity were assessed during a 3-day inpatient stay. A fasted skeletal muscle biopsy was obtained to assess mitochondrial functions. C2C12 myoblasts were transfected with FLAG-HA-USP15 and FLAG-HA-USP30 and harvested to assess mitochondrial dynamics and cellular insulin action.
resultsInsulin sensitivity and aerobic capacity were lower in Ow/Ob (132% and 28%, respectively) and T2D (1024% and 83%, respectively) relative to HW. Patients with T2D presented with elevated skeletal muscle mitochondrial fission (3.2 fold relative to HW and Ow/Ob), decreased fusion, and impairments in quality control. Mitochondrial content was lower in Ow/Ob (26%) and T2D (56%). USP13 (84%), USP15 (96%) and USP30 (53%) expression were increased with decreased Parkin and Ub activation in T2D alone. USP15 (R
conclusionMitochondrial fragmentation bypasses defects in mitophagy to sustain skeletal muscle quality control in patients with T2D.
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