ArticleJournal of translational medicine2013
Oxidative damage and myofiber degeneration in the gastrocnemius of patients with peripheral arterial disease.
Article in Journal of translational medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sarcopenia and peripheral arterial disease: a systematic review.Journal of cachexia, sarcopenia and muscle · 2020Pooled it
- Nicotinamide riboside for peripheral artery disease: the NICE randomized clinical trial.Nature communications · 2024Trial
- Cocoa flavanols, Nrf2 activation, and oxidative stress in peripheral artery disease: mechanistic findings in muscle based on outcomes from a randomized trial.American journal of physiology. Cell physiology · 2024Trial
- Chronic Limb-Threatening Ischemia Shows No Adaptability of Mitochondrial Function After Revascularisation.Journal of cellular and molecular medicine · 2026Article
- Cilostazol use and calf muscle pathophysiology in people with peripheral artery disease.Vascular medicine (London, England) · 2026Article
- Article
- Ferroptosis-related stress during aging and its relevance to disease.GeroScience · 2026Review
- Research Progress on the Association Between Sarcopenic Obesity and Atherosclerosis: Current Status and Challenges.Journal of clinical medicine · 2025Review
- Gastrocnemius Myofiber Type and Mitochondrial Alterations Associated With Peripheral Artery Disease Severity.Function (Oxford, England) · 2025Article
- NIR light-propelled Janus Polydopamine@Mesoporous silica gene delivery nanomotor for the enhanced gene treatment of critical limb ischemia.Materials today. Bio · 2025Article
- New horizons in nuclear cardiology: Imaging of peripheral arterial disease.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2025Review
- Chronic alcohol consumption exacerbates ischemia-associated skeletal muscle mitochondrial dysfunction in a murine model of peripheral artery disease.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Skeletal muscle desmin alterations following revascularization in peripheral artery disease claudicants.Scientific reports · 2024Article
- Inflammatory Cells in Adipose Tissue and Skeletal Muscle of Patients with Peripheral Arterial Disease or Chronic Venous Disease: A Prospective, Observational, and Histological Study.Journal of cardiovascular development and disease · 2024Article
- Oxidative damage in the gastrocnemius predicts long-term survival in patients with peripheral artery disease.npj aging · 2024Article
- Mitochondrial respiration in peripheral arterial disease depends on stage severity.Journal of cellular and molecular medicine · 2024Article
- Ultrastructural alterations and mitochondrial dysfunction in skeletal muscle of peripheral artery disease patients: implications for early therapeutic interventions.EXCLI journal · 2024Article
- Diet-induced obesity augments ischemic myopathy and functional decline in a murine model of peripheral artery disease.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Diabetes mellitus in peripheral artery disease: Beyond a risk factor.Frontiers in cardiovascular medicine · 2023Review
- Dysregulated Genes, MicroRNAs, Biological Pathways, and Gastrocnemius Muscle Fiber Types Associated With Progression of Peripheral Artery Disease: A Preliminary Analysis.Journal of the American Heart Association · 2022Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors.
Funding
Abstract
Peripheral arterial disease (PAD), a manifestation of systemic atherosclerosis that produces blockages in arteries supplying the legs, affects an estimated 27 million people in Europe and North America. Increased production of reactive oxygen species by dysfunctional mitochondria in leg muscles of PAD patients is viewed as a key mechanism of initiation and progression of the disease. Previous studies demonstrated increased oxidative damage in homogenates of biopsy specimens from PAD gastrocnemius compared to controls, but did not address myofiber-specific damage. In this study, we investigated oxidative damage to myofibers as a possible cause of the myopathy of PAD. To achieve this, we developed and validated fluorescence microscopy procedures for quantitative analysis of carbonyl groups and 4-hydroxy-2-nonenal (HNE) adducts in myofibers of biopsy specimens from human gastrocnemius. PAD and control specimens were evaluated for differences in 1) myofiber content of these two forms of oxidative damage and 2) myofiber cross-sectional area. Furthermore, oxidative damage to PAD myofibers was tested for associations with clinical stage of disease, degree of ischemia in the affected leg, and myofiber cross-sectional area. Carbonyl groups and HNE adducts were increased 30% (p < 0.0001) and 40% (p < 0.0001), respectively, in the myofibers of PAD (N = 34) compared to control (N = 21) patients. Mean cross-sectional area of PAD myofibers was reduced 29.3% compared to controls (p < 0.0003). Both forms of oxidative damage increased with clinical stage of disease, blood flow limitation in the ischemic leg, and reduced myofiber cross-sectional area. The data establish oxidative damage to myofibers as a possible cause of PAD myopathy.
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