ArticleFree radical biology & medicine2014
Monoamine oxidase inhibition prevents mitochondrial dysfunction and apoptosis in myoblasts from patients with collagen VI myopathies.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- Selegiline, a monoamine oxidase-B inhibitor as a modulator of metabolic reprogramming for cancer therapy: a review.Frontiers in pharmacology · 2026Review
- Modulating autism spectrum disorder pathophysiology using a trace amine-focused approach: targeting the gut.Molecular medicine (Cambridge, Mass.) · 2025Review
- Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.Physiological research · 2024Review
- Type-B monoamine oxidase inhibitors in neurological diseases: clinical applications based on preclinical findings.Neural regeneration research · 2024Review
- Inhibition of monoamine oxidase-a increases respiration in isolated mouse cortical mitochondria.Experimental neurology · 2023Article
- Collagen VI in the Musculoskeletal System.International journal of molecular sciences · 2023Review
- Potential contributions of trace amines in Alzheimer's disease and therapeutic prospects.Neural regeneration research · 2021Article
- The Determining Role of Mitochondrial Reactive Oxygen Species Generation and Monoamine Oxidase Activity in Doxorubicin-Induced Cardiotoxicity.Antioxidants & redox signaling · 2021Article
- Multiparametric Monitoring of Hypnosis and Nociception-Antinociception Balance during General Anesthesia-A New Era in Patient Safety Standards and Healthcare Management.Medicina (Kaunas, Lithuania) · 2021Review
- Linking Oxidative Stress and DNA Damage to Changes in the Expression of Extracellular Matrix Components.Frontiers in genetics · 2021Review
- Reactive Oxygen Species and Oxidative Stress in the Pathogenesis and Progression of Genetic Diseases of the Connective Tissue.Antioxidants (Basel, Switzerland) · 2020Review
- Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.Antioxidants (Basel, Switzerland) · 2020Review
- Teaching an Old Molecule New Tricks: Drug Repositioning for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- Compromised Exercise Capacity and Mitochondrial Dysfunction in the Osteogenesis Imperfecta Murine (oim) Mouse Model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019Article
- Drug Repurposing for Duchenne Muscular Dystrophy: The Monoamine Oxidase B Inhibitor Safinamide Ameliorates the Pathological Phenotype inFrontiers in physiology · 2018Article
- Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.International review of cell and molecular biology · 2018Review
- Denervated muscle fibers induce mitochondrial peroxide generation in neighboring innervated fibers: Role in muscle aging.Free radical biology & medicine · 2017Article
- Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies.Oxidative medicine and cellular longevity · 2016Review
- Pharmacology and Clinical Drug Candidates in Redox Medicine.Antioxidants & redox signaling · 2015Review
- Rasagiline and selegiline suppress calcium efflux from mitochondria by PK11195-induced opening of mitochondrial permeability transition pore: a novel anti-apoptotic function for neuroprotection.Journal of neural transmission (Vienna, Austria : 1996) · 2015Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Although mitochondrial dysfunction and oxidative stress have been proposed to play a crucial role in several types of muscular dystrophy (MD), whether a causal link between these two alterations exists remains an open question. We have documented that mitochondrial dysfunction through opening of the permeability transition pore plays a key role in myoblasts from patients as well as in mouse models of MD, and that oxidative stress caused by monoamine oxidases (MAO) is involved in myofiber damage. In the present study we have tested whether MAO-dependent oxidative stress is a causal determinant of mitochondrial dysfunction and apoptosis in myoblasts from patients affected by collagen VI myopathies. We find that upon incubation with hydrogen peroxide or the MAO substrate tyramine myoblasts from patients upregulate MAO-B expression and display a significant rise in reactive oxygen species (ROS) levels, with concomitant mitochondrial depolarization. MAO inhibition by pargyline significantly reduced both ROS accumulation and mitochondrial dysfunction, and normalized the increased incidence of apoptosis in myoblasts from patients. Thus, MAO-dependent oxidative stress is causally related to mitochondrial dysfunction and cell death in myoblasts from patients affected by collagen VI myopathies, and inhibition of MAO should be explored as a potential treatment for these diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.