ArticleMolecular and cellular biology2004
The CRM1 nuclear export receptor controls pathological cardiac gene expression.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 0 citations in OpenAlex.
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- HDAC5 promotes optic nerve regeneration by activating the mTOR pathway.Experimental neurology · 2019Article
- A CRM1 Inhibitor Alleviates Cardiac Hypertrophy and Increases the Nuclear Distribution of NT-PGC-1α in NRVMs.Frontiers in pharmacology · 2019Article
- β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation.Journal of the American Heart Association · 2017Article
- Local TNF causes NFATc1-dependent cholesterol-mediated podocyte injury.The Journal of clinical investigation · 2016Article
- A class of their own: exploring the nondeacetylase roles of class IIa HDACs in cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2016Review
- F-BOX proteins in cancer cachexia and muscle wasting: Emerging regulators and therapeutic opportunities.Seminars in cancer biology · 2016Review
- Role of Mitochondrial RNA Polymerase in the Toxicity of Nucleotide Inhibitors of Hepatitis C Virus.Antimicrobial agents and chemotherapy · 2016Article
- Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy.Cell metabolism · 2015Article
- Roles and post-translational regulation of cardiac class IIa histone deacetylase isoforms.The Journal of physiology · 2015Review
- Nuclear pore rearrangements and nuclear trafficking in cardiomyocytes from rat and human failing hearts.Cardiovascular research · 2015Article
- Class I and IIa histone deacetylases have opposite effects on sclerostin gene regulation.The Journal of biological chemistry · 2014Article
- Histone deacetylase signaling in cardioprotection.Cellular and molecular life sciences : CMLS · 2014Review
- Four-and-a-half LIM domains proteins are novel regulators of the protein kinase D pathway in cardiac myocytes.The Biochemical journal · 2014Article
- Estrogen regulates histone deacetylases to prevent cardiac hypertrophy.Molecular biology of the cell · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diverse pathological insults trigger a cardiac remodeling process during which myocytes undergo hypertrophy, with consequent decline in cardiac function and eventual heart failure. Multiple transcriptional regulators of pathological cardiac hypertrophy are controlled at the level of subcellular distribution. For example, prohypertrophic transcription factors belonging to the nuclear factor of activated T cells (NFAT) and GATA families are subject to CRM1-dependent nuclear export but are rapidly relocalized to the nucleus in response to cues for hypertrophic growth. Here, we demonstrate that the antihypertrophic chromatin-modifying enzyme histone deacetylase 5 (HDAC5) is shuttled out of the cardiomyocyte nucleus via a CRM1-mediated pathway in response to diverse signals for hypertrophy. CRM1 antagonists block the agonist-mediated nuclear export of HDAC 5 and repress pathological gene expression and associated hypertrophy of cultured cardiomyocytes. Conversely, CRM1 activity is dispensable for nonpathological cardiac gene activation mediated by thyroid hormone and insulin-like growth factor 1, agonists that fail to trigger the nuclear export of HDAC5. These results suggest a selective role for CRM1 in derepression of pathological cardiac genes via its neutralizing effects on antihypertrophic factors such as HDAC5. Pharmacological approaches targeting CRM1-dependent nuclear export in heart muscle may have salutary effects on cardiac function by suppressing maladaptive changes in gene expression evoked by stress signals.
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