ArticleOrphanet journal of rare diseases2020
Cardiovascular progenitor cells and tissue plasticity are reduced in a myocardium affected by Becker muscular dystrophy.
Article in Orphanet journal of rare diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Mexico's First Heart Transplant in a Patient with Becker Muscular Dystrophy Reveals an Overlooked Cause of Idiopathic Dilated Cardiomyopathy.Muscles (Basel, Switzerland) · 2026Article
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
- Dystrophin Deficiency Causes Progressive Depletion of Cardiovascular Progenitor Cells in the Heart.International journal of molecular sciences · 2021Article
- Quantitative assessment of left ventricular longitudinal function and myocardial deformation in Duchenne muscular dystrophy patients.Orphanet journal of rare diseases · 2021Article
- Echocardiographic signs of subclinical cardiac function impairment in Duchenne dystrophy gene carriers.Scientific reports · 2020Article
- DMD Pluripotent Stem Cell Derived Cardiac Cells RecapitulateFrontiers in bioengineering and biotechnology · 2020Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
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Abstract
We describe the association of Becker muscular dystrophy (BMD) derived heart failure with the impairment of tissue homeostasis and remodeling capabilities of the affected heart tissue. We report that BMD heart failure is associated with a significantly decreased number of cardiovascular progenitor cells, reduced cardiac fibroblast migration, and ex vivo survival.
backgroundBecker muscular dystrophy belongs to a class of genetically inherited dystrophin deficiencies. It affects male patients and results in progressive skeletal muscle degeneration and dilated cardiomyopathy leading to heart failure. It is a relatively mild form of dystrophin deficiency, which allows patients to be on a heart transplant list. In this unique situation, the explanted heart is a rare opportunity to study the degenerative process of dystrophin-deficient cardiac tissue. Heart tissue was excised, dissociated, and analyzed. The fractional content of c-kit
resultsWe report significantly decreased CVPCs (c-kit
conclusionsOur findings associate genetically derived heart failure in a dystrophin-deficient patient with decreased c-kit
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