ArticleCell calcium2015
Mitochondrial dysfunctions during progression of dystrophic cardiomyopathy.
Article in Cell calcium, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- NLRX1 emerges as the only observed essential regulator of the mPTP, challenging mPTP inhibition as a valid target of cardioprotection.Basic research in cardiology · 2026Review
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Targeting autophagy in Duchenne muscular dystrophy: mechanistic insights and emerging therapeutic strategies.Journal of medical genetics · 2026Review
- Cardiomyoprotective effect of Tanshinone IIA in diabetic cardiomyopathy achieved through enhancing PINK1-Parkin dependent mitophagy.Histology and histopathology · 2026Article
- Potential Involvement of Ferroptosis in Duchenne Muscular Dystrophy-Associated Cardiomyopathy.Biomedicines · 2026Article
- Cardiovascular remodeling: key mechanisms and clinical implications linking sarcopenia and heart failure.Frontiers in medicine · 2026Review
- Quantitative proteomics analysis reveals the pathogenesis of obstructed defecation syndrome caused by abnormal expression of dystrophin.World journal of gastroenterology · 2024Article
- Review
- Improved mitochondrial function in the hearts of sarcolipin-deficient dystrophin and utrophin double-knockout mice.JCI insight · 2024Article
- LED therapy plus idebenone treatment targeting calcium and mitochondrial signaling pathways in dystrophic muscle cells.Cell stress & chaperones · 2023Article
- RANKL Inhibition Reduces Cardiac Hypertrophy inCells · 2023Article
- Deficiency of mitochondrial calcium uniporter abrogates iron overload-induced cardiac dysfunction by reducing ferroptosis.Basic research in cardiology · 2023Article
- Modeling Duchenne Muscular Dystrophy Cardiomyopathy with Patients' Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2023Review
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- Mitochonic Acid 5 Improves Duchenne Muscular Dystrophy and Parkinson's Disease Model ofInternational journal of molecular sciences · 2022Article
- The Remaining Conundrum of the Role of the NaReviews in cardiovascular medicine · 2022Review
- The Role of Taurine in Skeletal Muscle Functioning and Its Potential as a Supportive Treatment for Duchenne Muscular Dystrophy.Metabolites · 2022Review
- Reducing sarcolipin expression improves muscle metabolism inAmerican journal of physiology. Cell physiology · 2022Article
- Cardiomyocyte-produced miR-339-5p mediates pathology in Duchenne muscular dystrophy cardiomyopathy.Human molecular genetics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a progressive muscle disease with severe cardiac complications. It is believed that cellular oxidative stress and augmented Ca(2+) signaling drives the development of cardiac pathology. Some mitochondrial and metabolic dysfunctions have also been reported. Here we investigate cellular mechanisms responsible for impaired mitochondrial metabolism in dystrophic cardiomyopathy at early stages of the disease. We employed electrophysiological and imaging techniques to study mitochondrial structure and function in cardiomyocytes from mdx mice, an animal model of DMD. Here we show that mitochondrial matrix was progressively oxidized in myocytes isolated from mdx mice. Moreover, an abrupt increase in workload resulted in significantly more pronounced oxidation of mitochondria in dystrophic cells. Electron micrographs revealed a gradually increased number of damaged mitochondria in mdx myocytes. Degradation in mitochondrial structure was correlated with progressive increase in mitochondrial Ca(2+) sequestration and mitochondrial depolarization, despite a substantial and persistent elevation in resting cytosolic sodium levels. Treatment of mdx cells with cyclosporine A, an inhibitor of mitochondrial permeability transition pore (mPTP), shifted both resting and workload-dependent mitochondrial redox state to the levels recorded in control myocytes. It also significantly reduced workload dependent depolarization of mitochondrial membrane in dystrophic cardiomyocytes. Overall, our studies highlight age dependent deterioration of mitochondrial function in dystrophic cardiomyocytes, which seems to be associated with excessive opening of mPTP due to oxidative stress and cellular Ca(2+) overload.
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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.