ArticleCardiovascular research2013
Inducible re-expression of HEXIM1 causes physiological cardiac hypertrophy in the adult mouse.
Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- cGAS/STING-Independent Induction of Type I Interferon by Inhibitors of the Histone Methylase KDM5B.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure.Frontiers in cardiovascular medicine · 2019Review
- Induction of HEXIM1 activities by HMBA derivative 4a1: Functional consequences and mechanism.Cancer letters · 2016Article
- Overexpression of miR-223 Tips the Balance of Pro- and Anti-hypertrophic Signaling Cascades toward Physiologic Cardiac Hypertrophy.The Journal of biological chemistry · 2016Article
- Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation.Cell communication and signaling : CCS · 2014Article
- BET-ting on chromatin-based therapeutics for heart failure.Journal of molecular and cellular cardiology · 2014Review
- Triggering the succinate receptor GPR91 enhances pressure overload-induced right ventricular hypertrophy.International journal of clinical and experimental pathology · 2014Article
- The G4 resolvase RHAU modulates mRNA translation and stability to sustain postnatal heart function and regeneration.The Journal of biological chemistryArticle
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
aimsThe transcription factor hexamethylene-bis-acetamide-inducible protein 1 (HEXIM1) regulates myocardial vascularization and growth during cardiogenesis. Our aim was to determine whether HEXIM1 also has a beneficial role in modulating vascularization, myocardial growth, and function within the adult heart. METHODS AND
resultsTo achieve our objective, we created and investigated a mouse line wherein HEXIM1 was re-expressed in adult cardiomyocytes to levels found in the foetal heart. Our findings support a beneficial role for HEXIM1 through increased vascularization, myocardial growth, and increased ejection fraction within the adult heart. HEXIM1 re-expression induces angiogenesis, that is, essential for physiological hypertrophy and maintenance of cardiac function. The ability of HEXIM1 to co-ordinate processes associated with physiological hypertrophy may be attributed to HEXIM1 regulation of other transcription factors (HIF-1-α, c-Myc, GATA4, and PPAR-α) that, in turn, control many genes involved in myocardial vascularization, growth, and metabolism. Moreover, the mechanism for HEXIM1-induced physiological hypertrophy appears to be distinct from that involving the PI3K/AKT pathway.
conclusionHEXIM1 re-expression results in the induction of angiogenesis that allows for the co-ordination of tissue growth and angiogenesis during physiological hypertrophy.
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Registered trials
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