ArticlePloS one2012
Deep RNA sequencing reveals novel cardiac transcriptomic signatures for physiological and pathological hypertrophy.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 96 citations in OpenAlex.
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- Mycn ameliorates cardiac hypertrophy-induced heart failure in mice by mediating the USP2/JUP/Akt/β-catenin cascade.BMC cardiovascular disorders · 2024Article
- Cardiac splicing as a diagnostic and therapeutic target.Nature reviews. Cardiology · 2023Review
- Circ-Ddx60 contributes to the antihypertrophic memory of exercise hypertrophic preconditioning.Journal of advanced research · 2023Article
- Integrated Quantitative Phosphoproteomics and Cell-based Functional Screening Reveals Specific Pathological Cardiac Hypertrophy-related Phosphorylation Sites.Molecules and cells · 2021Article
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- Maternal obesity persistently alters cardiac progenitor gene expression and programs adult-onset heart disease susceptibility.Molecular metabolism · 2021Article
- The Role of Exercise-Induced Molecular Processes and Vitamin D in Improving Cardiorespiratory Fitness and Cardiac Rehabilitation in Patients With Heart Failure.Frontiers in physiology · 2021Review
- Multidimensional Mechanistic Spectrum of Long Non-coding RNAs in Heart Development and Disease.Frontiers in cardiovascular medicine · 2021Review
- RCAN1 in cardiovascular diseases: molecular mechanisms and a potential therapeutic target.Molecular medicine (Cambridge, Mass.) · 2020Review
- Exercise and cardiac health: physiological and molecular insights.Nature metabolism · 2020Review
- Sexual dimorphism in cardiac transcriptome associated with a troponin C murine model of hypertrophic cardiomyopathy.Physiological reports · 2020Article
- The Mechanism of High-Output Cardiac Hypertrophy Arising From Potassium Channel Gain-of-Function in Cantú Syndrome.Function (Oxford, England) · 2020Article
- Energy Metabolism in Exercise-Induced Physiologic Cardiac Hypertrophy.Frontiers in pharmacology · 2020Review
- Transcriptomics of cardiac biopsies reveals differences in patients with or without diagnostic parameters for heart failure with preserved ejection fraction.Scientific reports · 2019Article
- Weighted Gene Co-Expression Network Analysis Identifies Critical Genes in the Development of Heart Failure After Acute Myocardial Infarction.Frontiers in genetics · 2019Article
- Vegfc/d-dependent regulation of the lymphatic vasculature during cardiac regeneration is influenced by injury context.NPJ Regenerative medicine · 2019Article
- A novel system-level approach using RNA-sequencing data identifies miR-30-5p and miR-142a-5p as key regulators of apoptosis in myocardial infarction.Scientific reports · 2018Article
- Differentially Expressed Genes Associated with the Cabbage Yellow-Green-Leaf Mutant in theInternational journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although both physiological hypertrophy (PHH) and pathological hypertrophy (PAH) of the heart have similar morphological appearances, only PAH leads to fatal heart failure. In the present study, we used RNA sequencing (RNA-Seq) to determine the transcriptomic signatures for both PHH and PAH. Approximately 13-20 million reads were obtained for both models, among which PAH showed more differentially expressed genes (DEGs) (2,041) than PHH (245). The expression of 417 genes was barely detectable in the normal heart but was suddenly activated in PAH. Among them, Foxm1 and Plk1 are of particular interest, since Ingenuity Pathway Analysis (IPA) using DEGs and upstream motif analysis showed that they are essential hub proteins that regulate the expression of downstream proteins associated with PAH. Meanwhile, 52 genes related to collagen, chemokines, and actin showed opposite expression patterns between PHH and PAH. MAZ-binding motifs were enriched in the upstream region of the participating genes. Alternative splicing (AS) of exon variants was also examined using RNA-Seq data for PAH and PHH. We found 317 and 196 exon inclusions and exon exclusions, respectively, for PAH, and 242 and 172 exon inclusions and exclusions, respectively for PHH. The AS pattern was mostly related to gains or losses of domains, changes in activity, and localization of the encoded proteins. The splicing variants of 8 genes (i.e., Fhl1, Rcan1, Ndrg2, Synpo, Ttll1, Cxxc5, Egfl7, and Tmpo) were experimentally confirmed. Multilateral pathway analysis showed that the patterns of quantitative (DEG) and qualitative (AS) changes differ depending on the type of pathway in PAH and PHH. One of the most significant changes in PHH is the severe downregulation of autoimmune pathways accompanied by significant AS. These findings revealed the unique transcriptomic signatures of PAH and PHH and also provided a more comprehensive understanding at both the quantitative and qualitative levels.
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