ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Hypersensitivity of excitation-contraction coupling in dystrophic cardiomyocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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33 citing papers in PubMed, 50 citations in OpenAlex.
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- Calcium handling maturation and adaptation to increased substrate stiffness in human iPSC-derived cardiomyocytes: The impact of full-length dystrophin deficiency.Frontiers in physiology · 2022Article
- Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences.International journal of molecular sciences · 2021Review
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- The molecular mechanisms associated with the physiological responses to inflammation and oxidative stress in cardiovascular diseases.Biophysical reviews · 2020Review
- Prevention of connexin-43 remodeling protects against Duchenne muscular dystrophy cardiomyopathy.The Journal of clinical investigation · 2020Article
- Dysregulation of Calcium Handling in Duchenne Muscular Dystrophy-Associated Dilated Cardiomyopathy: Mechanisms and Experimental Therapeutic Strategies.Journal of clinical medicine · 2020Review
- 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
- Research progress on the role of CaMKII in heart disease.American journal of translational research · 2020Review
- Elimination of fukutin reveals cellular and molecular pathomechanisms in muscular dystrophy-associated heart failure.Nature communications · 2019Article
- Dystrophin deficiency leads to dysfunctional glutamate clearance in iPSC derived astrocytes.Translational psychiatry · 2019Article
- Exacerbation of dystrophic cardiomyopathy by phospholamban deficiency mediated chronically increased cardiac CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Voltage-Dependent Sarcolemmal Ion Channel Abnormalities in the Dystrophin-Deficient Heart.International journal of molecular sciences · 2018Review
- Oxidized CaMKII (CaCirculation. Arrhythmia and electrophysiology · 2018Article
- Calcium Uncaging with Visible Light.Journal of the American Chemical Society · 2016Article
- Pivotal role of miR-448 in the development of ROS-induced cardiomyopathy.Cardiovascular research · 2015Article
- A change of heart: oxidative stress in governing muscle function?Biophysical reviews · 2015Article
- Oxidative stress and ca(2+) release events in mouse cardiomyocytes.Biophysical journal · 2014Article
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5 authors at 2 institutions in 2 countries.
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Abstract
Duchenne muscular dystrophy represents a severe inherited disease of striated muscle. It is caused by a mutation of the dystrophin gene and characterized by a progressive loss of skeletal muscle function. Most patients also develop a dystrophic cardiomyopathy, resulting in dilated hypertrophy and heart failure, but the cellular mechanisms leading to the deterioration of cardiac function remain elusive. In the present study, we tested whether defective excitation-contraction (E-C) coupling contributes to impaired cardiac performance. "E-C coupling gain" was determined in cardiomyocytes from control and dystrophin-deficient mdx mice. To this end, L-type Ca2+ currents (ICaL) were measured with the whole cell patch-clamp technique, whereas Ca2+ transients were simultaneously recorded with confocal imaging of fluo-3. Initial findings indicated subtle changes of E-C coupling in mdx cells despite matched Ca2+ loading of the sarcoplasmic reticulum (SR). However, lowering the extracellular Ca2+ concentration, a maneuver used to unmask latent E-C coupling problems, was surprisingly much better tolerated by mdx myocytes, suggesting a hypersensitive E-C coupling mechanism. Challenging the SR Ca2+ release by slow elevations of the intracellular Ca2+ concentration resulted in Ca2+ oscillations after a much shorter delay in mdx cells. This is consistent with an enhanced Ca2+ sensitivity of the SR Ca2+-release channels [ryanodine receptors (RyRs)]. The hypersensitivity could be normalized by the introduction of reducing agents, indicating that the elevated cellular ROS generation in dystrophy underlies the abnormal RyR sensitivity and hypersensitive E-C coupling. Our data suggest that in dystrophin-deficient cardiomyocytes, E-C coupling is altered due to potentially arrhythmogenic changes in the Ca2+ sensitivity of redox-modified RyRs.
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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.