ArticleJournal of molecular and cellular cardiology2013
Sequencing of mRNA identifies re-expression of fetal splice variants in cardiac hypertrophy.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- RNA splicing and cardiovascular disease: a guide for cardiologists.European heart journal · 2026Review
- Transcriptional regulation in heart development, disease and regeneration: reassessing the fetal gene hypothesis.Nature reviews. Cardiology · 2026Review
- Alternative splicing of the Snap23 microexon is regulated by MBNL, QKI, and RBFOX2 in a tissue-specific manner and is altered in striated muscle diseases.RNA biology · 2025Article
- Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during mouse fetal heart development.Developmental cell · 2023Article
- Alternative splicing regulation of membrane trafficking genes during myogenesis.RNA (New York, N.Y.) · 2022Article
- Dissecting the transcriptome in cardiovascular disease.Cardiovascular research · 2022Review
- Review
- Scaffold-Mediated Developmental Effects on Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes Are Preserved After External Support Removal.Frontiers in cell and developmental biology · 2021Article
- DAND5 Inactivation Enhances Cardiac Differentiation in Mouse Embryonic Stem Cells.Frontiers in cell and developmental biology · 2021Article
- Intronic Determinants Coordinate Charme lncRNA Nuclear Activity through the Interaction with MATR3 and PTBP1.Cell reports · 2020Article
- RNA-Binding Proteins in Pulmonary Hypertension.International journal of molecular sciences · 2020Review
- Dynamic Transcriptional Responses to Injury of Regenerative and Non-regenerative Cardiomyocytes Revealed by Single-Nucleus RNA Sequencing.Developmental cell · 2020Article
- Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro.Nature communications · 2019Article
- Genetic and epigenetic regulation of cardiomyocytes in development, regeneration and disease.Development (Cambridge, England) · 2018Review
- Alternative splicing in cardiomyopathy.Biophysical reviews · 2018Review
- LOX-1 and Its Splice Variants: A New Challenge for Atherosclerosis and Cancer-Targeted Therapies.International journal of molecular sciences · 2017Review
- Neonatal cardiac dysfunction and transcriptome changes caused by the absence of Celf1.Scientific reports · 2016Article
- Genome-wide analysis of alternative splicing during human heart development.Scientific reports · 2016Article
- Calcific Aortic Valve Disease: Part 2-Morphomechanical Abnormalities, Gene Reexpression, and Gender Effects on Ventricular Hypertrophy and Its Reversibility.Journal of cardiovascular translational research · 2016Review
- Loss of muscleblind-like 1 results in cardiac pathology and persistence of embryonic splice isoforms.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac hypertrophy has been well-characterized at the level of transcription. During cardiac hypertrophy, genes normally expressed primarily during fetal heart development are re-expressed, and this fetal gene program is believed to be a critical component of the hypertrophic process. Recently, alternative splicing of mRNA transcripts has been shown to be temporally regulated during heart development, leading us to consider whether fetal patterns of splicing also reappear during hypertrophy. We hypothesized that patterns of alternative splicing occurring during heart development are recapitulated during cardiac hypertrophy. Here we present a study of isoform expression during pressure-overload cardiac hypertrophy induced by 10 days of transverse aortic constriction (TAC) in rats and in developing fetal rat hearts compared to sham-operated adult rat hearts, using high-throughput sequencing of poly(A) tail mRNA. We find a striking degree of overlap between the isoforms expressed differentially in fetal and pressure-overloaded hearts compared to control: forty-four percent of the isoforms with significantly altered expression in TAC hearts are also expressed at significantly different levels in fetal hearts compared to control (P<0.001). The isoforms that are shared between hypertrophy and fetal heart development are significantly enriched for genes involved in cytoskeletal organization, RNA processing, developmental processes, and metabolic enzymes. Our data strongly support the concept that mRNA splicing patterns normally associated with heart development recur as part of the hypertrophic response to pressure overload. These findings suggest that cardiac hypertrophy shares post-transcriptional as well as transcriptional regulatory mechanisms with fetal heart development.
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Registered trials
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