ArticleOxidative medicine and cellular longevity2015
Oxidative Stress in Dilated Cardiomyopathy Caused by MYBPC3 Mutation.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- SGLT2 Inhibitors in Hypertrophic Cardiomyopathy: Emerging Evidence and Putative Mechanisms.Biomolecules · 2026Review
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- The Pathogenic Role of the DNA Double-Stranded Breaks in Hereditary Cardiomyopathies.Heart failure clinics · 2026Review
- Electron paramagnetic resonance spectroscopy for analysis of free radicals in zebrafish.PloS one · 2025Article
- Multi-Omics Profiling of Hypertrophic Cardiomyopathy Reveals Altered Mechanisms in Mitochondrial Dynamics and Excitation-Contraction Coupling.International journal of molecular sciences · 2023Article
- Clonal haematopoiesis of indeterminate potential-related mutations and outcome in dilated and ischaemic cardiomyopathy.ESC heart failure · 2022Article
- Article
- miR-16-5p Suppression Protects Human Cardiomyocytes against Endoplasmic Reticulum and Oxidative Stress-Induced Injury.International journal of molecular sciences · 2022Article
- Heterogeneous Distribution of Genetic Mutations in Myosin Binding Protein-C Paralogs.Frontiers in genetics · 2022Article
- Identification and Verification of Feature Biomarkers Associated With Immune Cells in Dilated Cardiomyopathy by Bioinformatics Analysis.Frontiers in genetics · 2022Article
- Integration of Cardiac Actin Mutants Causing Hypertrophic (p.A295S) and Dilated Cardiomyopathy (p.R312H and p.E361G) into Cellular Structures.Antioxidants (Basel, Switzerland) · 2021Article
- Double overexpression of miR-19a and miR-20a in induced pluripotent stem cell-derived mesenchymal stem cells effectively preserves the left ventricular function in dilated cardiomyopathic rat.Stem cell research & therapy · 2021Article
- Mass Spectrometry-Based Redox and Protein Profiling of Failing Human Hearts.International journal of molecular sciences · 2021Article
- SOD2 deficiency in cardiomyocytes defines defective mitochondrial bioenergetics as a cause of lethal dilated cardiomyopathy.Redox biology · 2020Article
- The potential roles of Von Willebrand factor and neutrophil extracellular traps in the natural history of hypertrophic and hypertensive cardiomyopathy.Thrombosis research · 2020Review
- Nitrite attenuates mitochondrial impairment and vascular permeability induced by ischemia-reperfusion injury in the lung.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Metabolic Alterations in Inherited Cardiomyopathies.Journal of clinical medicine · 2019Review
- Altered C10 domain in cardiac myosin binding protein-C results in hypertrophic cardiomyopathy.Cardiovascular research · 2019Article
- Hypertrophic Cardiomyopathy: A Vicious Cycle Triggered by Sarcomere Mutations and Secondary Disease Hits.Antioxidants & redox signaling · 2019Review
- Palbociclib improves cardiac dysfunction in diabetic cardiomyopathy by regulating Rb phosphorylation.American journal of translational research · 2019Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
Abstract
Cardiomyopathies can result from mutations in genes encoding sarcomere proteins including MYBPC3, which encodes cardiac myosin binding protein-C (cMyBP-C). However, whether oxidative stress is augmented due to contractile dysfunction and cardiomyocyte damage in MYBPC3-mutated cardiomyopathies has not been elucidated. To determine whether oxidative stress markers were elevated in MYBPC3-mutated cardiomyopathies, a previously characterized 3-month-old mouse model of dilated cardiomyopathy (DCM) expressing a homozygous MYBPC3 mutation (cMyBP-C((t/t))) was used, compared to wild-type (WT) mice. Echocardiography confirmed decreased percentage of fractional shortening in DCM versus WT hearts. Histopathological analysis indicated a significant increase in myocardial disarray and fibrosis while the second harmonic generation imaging revealed disorganized sarcomeric structure and myocyte damage in DCM hearts when compared to WT hearts. Intriguingly, DCM mouse heart homogenates had decreased glutathione (GSH/GSSG) ratio and increased protein carbonyl and lipid malondialdehyde content compared to WT heart homogenates, consistent with elevated oxidative stress. Importantly, a similar result was observed in human cardiomyopathy heart homogenate samples. These results were further supported by reduced signals for mitochondrial semiquinone radicals and Fe-S clusters in DCM mouse hearts measured using electron paramagnetic resonance spectroscopy. In conclusion, we demonstrate elevated oxidative stress in MYPBC3-mutated DCM mice, which may exacerbate the development of heart failure.
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