ArticleiScience2021
Skeletal muscle proteomes reveal downregulation of mitochondrial proteins in transition from prediabetes into type 2 diabetes.
Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Quantitative interactome mapping of skeletal muscle insulin resistance.Molecular systems biology · 2026Article
- April In focus in HCB: skeletal muscle fibers.Histochemistry and cell biology · 2026Article
- Article
- Fibre morphology, intramyocellular lipid content and 3D capillary architecture in human postural, respiratory and locomotor muscles in type 2 diabetes mellitus.Histochemistry and cell biology · 2026Article
- Ampk alpha2 T172 activation dictates exercise performance and energy transduction in skeletal muscle.Science advances · 2026Article
- Microgravity as a translational model for metabolic dysfunction: implications for obesity, insulin resistance, steatotic liver and pancreatic diseases.Frontiers in endocrinology · 2026Review
- STX4 Is Indispensable for Mitochondrial Homeostasis in Skeletal Muscle.Journal of cachexia, sarcopenia and muscle · 2025Article
- Obesity and Exercise: New Insights and Perspectives.Endocrine reviews · 2025Review
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Dysregulated skeletal muscle myosin super-relaxation and energetics in male participants with type 2 diabetes mellitus.Diabetologia · 2025Article
- Fiber-specific differences in protein content of pathways related to mTORC1 signaling and oxidative metabolism in individuals with obesity.Scientific reports · 2025Article
- Skeletal muscle proteomics: considerations and opportunities.npj metabolic health and disease · 2025Review
- Multi-omics approaches for biomarker discovery and precision diagnosis of prediabetes.Frontiers in endocrinology · 2025Review
- Proteomics Analysis Provides Insights into the Role of Lipid Metabolism in T2DM-Related Sarcopenia.ACS omega · 2024Article
- The mitochondrial multi-omic response to exercise training across rat tissues.Cell metabolism · 2024Article
- Harnessing the power of proteomics in precision diabetes medicine.Diabetologia · 2024Review
- Mitochondrial Dysfunction, Oxidative Stress, and Inter-Organ Miscommunications in T2D Progression.International journal of molecular sciences · 2024Review
- Remodeling of the human skeletal muscle proteome found after long-term endurance training but not after strength training.iScience · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Toward Ameliorating Insulin Resistance: Targeting a Novel PAK1 Signaling Pathway Required for Skeletal Muscle Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle insulin resistance is a central defect in the pathogenesis of type 2 diabetes (T2D). Here, we analyzed skeletal muscle proteome in 148 vastus lateralis muscle biopsies obtained from men covering all glucose tolerance phenotypes: normal, impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and T2D. Skeletal muscle proteome was analyzed by a sequential window acquisition of all theoretical mass spectra (SWATH-MS) proteomics technique. Our data indicate a downregulation in several proteins involved in mitochondrial electron transport or respiratory chain complex assembly already in IFG and IGT muscles, with most profound decreases observed in T2D. Additional phosphoproteomic analysis reveals altered phosphorylation in several signaling pathways in IFG, IGT, and T2D muscles, including those regulating glucose metabolic processes, and the structure of muscle cells. These data reveal several alterations present in skeletal muscle already in prediabetes and highlight impaired mitochondrial energy metabolism in the trajectory from prediabetes into T2D.
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