ArticleAmerican journal of physiology. Heart and circulatory physiology2013
p90 ribosomal S6 kinase 3 contributes to cardiac insufficiency in α-tropomyosin Glu180Gly transgenic mice.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- AKAP6β-a conductor in the orchestra of pathological cardiomyocyte gene transcription.Molecular pharmacology · 2026Review
- Distribution of cardiomyocyte-selective adeno-associated virus serotype 9 vectors in swine following intracoronary and intravenous infusion.Physiological genomics · 2022Article
- RSK3 mediates necroptosis by regulating phosphorylation of RIP3 in rat retinal ganglion cells.Journal of anatomy · 2020Article
- mAKAPβ signalosomes - A nodal regulator of gene transcription associated with pathological cardiac remodeling.Cellular signalling · 2019Review
- Regulation of Neuronal Survival and Axon Growth by a Perinuclear cAMP Compartment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Muscle A-kinase-anchoring protein-β-bound calcineurin toggles active and repressive transcriptional complexes of myocyte enhancer factor 2D.The Journal of biological chemistry · 2019Article
- Long-Term Biased β-Arrestin Signaling Improves Cardiac Structure and Function in Dilated Cardiomyopathy.Circulation · 2017Article
- Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research.Molecular and cellular biochemistry · 2017Review
- RSK3 is required for concentric myocyte hypertrophy in an activated Raf1 model for Noonan syndrome.Journal of molecular and cellular cardiology · 2016Article
- RSK3: A regulator of pathological cardiac remodeling.IUBMB life · 2015Review
- mAKAP-a master scaffold for cardiac remodeling.Journal of cardiovascular pharmacology · 2015Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial interstitial fibrosis is an important contributor to the development of heart failure. Type 3 p90 ribosomal S6 kinase (RSK3) was recently shown to be required for concentric myocyte hypertrophy under in vivo pathological conditions. However, the role of RSK family members in myocardial fibrosis remains uninvestigated. Transgenic expression of α-tropomyosin containing a Glu180Gly mutation (TM180) in mice of a mixed C57BL/6:FVB/N background induces a cardiomyopathy characterized by a small left ventricle, interstitial fibrosis, and diminished systolic and diastolic function. Using this mouse model, we now show that RSK3 is required for the induction of interstitial fibrosis in vivo. TM180 transgenic mice were crossed to RSK3 constitutive knockout (RSK3(-/-)) mice. Although RSK3 knockout did not affect myocyte growth, the decreased cardiac function and mild pulmonary edema associated with the TM180 transgene were attenuated by RSK3 knockout. The improved cardiac function was consistent with reduced interstitial fibrosis in the TM180;RSK3(-/-) mice as shown by histology and gene expression analysis, including the decreased expression of collagens. The specific inhibition of RSK3 should be considered as a potential novel therapeutic strategy for improving cardiac function and the prevention of sudden cardiac death in diseases in which interstitial fibrosis contributes to the development of heart failure.
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