ArticleThe Journal of clinical investigation1997
Cardiac compartment-specific overexpression of a modified retinoic acid receptor produces dilated cardiomyopathy and congestive heart failure in transgenic mice.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 101 citations in OpenAlex.
- Long-Term Dystrophin Replacement Therapy in Duchenne Muscular Dystrophy Causes Cardiac Inflammation.JACC. Basic to translational science · 2025Article
- Beyond genomic studies of congenital heart defects through systematic modelling and phenotyping.Disease models & mechanisms · 2024Article
- Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy.Biomedicines · 2024Article
- Am80, a retinoic acid receptor agonist, activates the cardiomyocyte cell cycle and enhances engraftment in the heart.Stem cell reports · 2023Article
- Brain nuclear receptors and cardiovascular function.Cell & bioscience · 2023Review
- Basic Research Approaches to Evaluate Cardiac Arrhythmia in Heart Failure and Beyond.Frontiers in physiology · 2022Review
- 100-fold but not 50-fold dystrophin overexpression aggravates electrocardiographic defects in the mdx model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2016Article
- Heterogeneous activation of a slow myosin gene in proliferating myoblasts and differentiated single myofibers.Developmental biology · 2015Article
- Rodent models of heart failure: an updated review.Heart failure reviews · 2013Review
- Relaxant effect of all-trans-retinoic acid via NO-sGC-cGMP pathway and calcium-activated potassium channels in rat mesenteric artery.American journal of physiology. Heart and circulatory physiology · 2013Article
- Physiological and genomic consequences of adrenergic deficiency during embryonic/fetal development in mice: impact on retinoic acid metabolism.Physiological genomics · 2012Article
- Lost in transgenesis: a user's guide for genetically manipulating the mouse in cardiac research.Circulation research · 2012Review
- Retinoic acid signalling is activated in the postischemic heart and may influence remodelling.PloS one · 2012Article
- An introduction to murine models of atrial fibrillation.Frontiers in physiology · 2012Article
- Left ventricular remodeling in swine after myocardial infarction: a transcriptional genomics approach.Basic research in cardiology · 2011Article
- Gene expression profiling of dilated cardiomyopathy in older male EP4 knockout mice.American journal of physiology. Heart and circulatory physiology · 2010Article
- Challenges and opportunities in dystrophin-deficient cardiomyopathy gene therapy.Human molecular genetics · 2006Review
- Down-regulation of retinoic acid receptor alpha signaling is required for sacculation and type I cell formation in the developing lung.The Journal of biological chemistry · 2003Article
- Dilated cardiomyopathy in mice deficient for the lysosomal cysteine peptidase cathepsin L.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Progressive atrioventricular conduction defects and heart failure in mice expressing a mutant Csx/Nkx2.5 homeoprotein.The Journal of clinical investigation · 2001Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Retinoids play a critical role in cardiac morphogenesis. To examine the effects of excessive retinoid signaling on myocardial development, transgenic mice that overexpress a constitutively active retinoic acid receptor (RAR) controlled by either the alpha- or beta-myosin heavy chain (MyHC) promoter were generated. Animals carrying the alpha-MyHC-RAR transgene expressed RARs in embryonic atria and in adult atria and ventricles, but developed no signs of either malformations or disease. In contrast, beta-MyHC-RAR animals, where expression was activated in fetal ventricles, developed a dilated cardiomyopathy that varied in severity with transgene copy number. Characteristic postmortem lesions included biventricular chamber dilation and left atrial thrombosis; the incidence and severity of these lesions increased with increasing copy number. Transcript analyses showed that molecular markers of hypertrophy, alpha-skeletal actin, atrial natriuretic factor and beta-MyHC, were upregulated. Cardiac performance of transgenic hearts was evaluated using the isolated perfused working heart model as well as in vivo, by transthoracic M-mode echocardiography. Both analyses showed moderate to severe impairment of left ventricular function and reduced cardiac contractility. Thus, expression of a constitutively active RAR in developing atria and/ or in postnatal ventricles is relatively benign, while ventricular expression during gestation can lead to significant cardiac dysfunction.
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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.