ReviewJournal of molecular and cellular cardiology2010
Alterations in mitochondrial function as a harbinger of cardiomyopathy: lessons from the dystrophic heart.
Review in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Empagliflozin preserves cardiac function and modulates metabolism in a mouse model of Duchenne muscular dystrophy.bioRxiv : the preprint server for biology · 2026Article
- Review
- Recent Advances in Pre-Clinical Development of Adiponectin Receptor Agonist Therapies for Duchenne Muscular Dystrophy.Biomedicines · 2024Review
- Right ventricular preload and afterload challenge induces contractile dysfunction and arrhythmia in isolated hearts of dystrophin-deficient male mice.Physiological reports · 2024Article
- Bioenergetic and Metabolic Impairments in Induced Pluripotent Stem Cell-Derived Cardiomyocytes Generated from Duchenne Muscular Dystrophy Patients.International journal of molecular sciences · 2022Article
- A medium-chain triglyceride containing ketogenic diet exacerbates cardiomyopathy in a CRISPR/Cas9 gene-edited rat model with Duchenne muscular dystrophy.Scientific reports · 2022Article
- Cardiac CIP protein regulates dystrophic cardiomyopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Metformin Reverses the Enhanced Myocardial SR/ER-Mitochondria Interaction and Impaired Complex I-Driven Respiration in Dystrophin-Deficient Mice.Frontiers in cell and developmental biology · 2020Article
- Metabolic Alterations in Cardiomyocytes of Patients with Duchenne and Becker Muscular Dystrophies.Journal of clinical medicine · 2019Review
- Voltage-Dependent Sarcolemmal Ion Channel Abnormalities in the Dystrophin-Deficient Heart.International journal of molecular sciences · 2018Review
- Exosome-Mediated Benefits of Cell Therapy in Mouse and Human Models of Duchenne Muscular Dystrophy.Stem cell reports · 2018Article
- Dystrophic Cardiomyopathy-Potential Role of Calcium in Pathogenesis, Treatment and Novel Therapies.Genes · 2017Review
- Mitochondrial dysfunctions during progression of dystrophic cardiomyopathy.Cell calcium · 2015Article
- Prevention of exercised induced cardiomyopathy following Pip-PMO treatment in dystrophic mdx mice.Scientific reports · 2015Article
- The Role of Cardiolipin in Cardiovascular Health.BioMed research international · 2015Review
- Article
- Disease-in-a-dish: the contribution of patient-specific induced pluripotent stem cell technology to regenerative rehabilitation.American journal of physical medicine & rehabilitation · 2014Review
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Exclusive skeletal muscle correction does not modulate dystrophic heart disease in the aged mdx model of Duchenne cardiomyopathy.Human molecular genetics · 2013Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
While compelling evidence supports the central role of mitochondrial dysfunction in the pathogenesis of heart failure, there is comparatively less information available on mitochondrial alterations that occur prior to failure. Building on our recent work with the dystrophin-deficient mdx mouse heart, this review focuses on how early changes in mitochondrial functional phenotype occur prior to overt cardiomyopathy and may be a determinant for the development of adverse cardiac remodelling leading to failure. These include alterations in energy substrate utilization and signalling of cell death through increased permeability of mitochondrial membranes, which may result from abnormal calcium handling, and production of reactive oxygen species. Furthermore, we will discuss evidence supporting the notion that these alterations in the dystrophin-deficient heart may represent an early "subclinical" signature of a defective nitric oxide/cGMP signalling pathway, as well as the potential benefit of mitochondria-targeted therapies. While the mdx mouse is an animal model of Duchenne muscular dystrophy (DMD), changes in the structural integrity of dystrophin, the mutated cytoskeletal protein responsible for DMD, have also recently been implicated as a common mechanism for contractile dysfunction in heart failure. In fact, altogether our findings support a critical role for dystrophin in maintaining optimal coupling between metabolism and contraction in the heart.
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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.