ArticleThe Journal of clinical investigation2007
Modulation of adverse cardiac remodeling by STARS, a mediator of MEF2 signaling and SRF activity.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 93 citations in OpenAlex.
- Effect of resistance exercise contraction mode and protein supplementation on members of the STARS signalling pathway.The Journal of physiology · 2013Trial
- Eccentric exercise activates novel transcriptional regulation of hypertrophic signaling pathways not affected by hormone changes.PloS one · 2010Trial
- Research progress on programmed cell death of cardiomyocytes in pressure-overload hypertrophic cardiomyopathy.Apoptosis : an international journal on programmed cell death · 2025Review
- The MEF2A transcription factor interactome in cardiomyocytes.Cell death & disease · 2023Article
- SRF: a seriously responsible factor in cardiac development and disease.Journal of biomedical science · 2022Review
- Isogenic human pluripotent stem cell disease models reveal ABRA deficiency underlies cTnT mutation-induced familial dilated cardiomyopathy.Protein & cell · 2022Article
- Molecular Mechanisms of Skeletal Muscle Hypertrophy.Journal of neuromuscular diseases · 2021Review
- Glucocorticoid Receptor-Binding and Transcriptome Signature in Cardiomyocytes.Journal of the American Heart Association · 2019Article
- Mechanosensitive Gene Regulation by Myocardin-Related Transcription Factors Is Required for Cardiomyocyte Integrity in Load-Induced Ventricular Hypertrophy.Circulation · 2018Article
- Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.Circulation · 2018Article
- Expression of striated activator of rho-signaling in human skeletal muscle following acute exercise and long-term training.Physiological reports · 2018Article
- Transcriptional and Post-Translational Targeting of Myocyte Stress Protein 1 (MS1) by the JNK Pathway in Cardiac Myocytes.Journal of molecular signaling · 2017Article
- Kainic Acid Induces mTORC1-Dependent Expression of Elmo1 in Hippocampal Neurons.Molecular neurobiology · 2017Article
- Z-disc protein CHAPb induces cardiomyopathy and contractile dysfunction in the postnatal heart.PloS one · 2017Article
- TRPC3-GEF-H1 axis mediates pressure overload-induced cardiac fibrosis.Scientific reports · 2016Article
- Myocardin-related transcription factors are required for skeletal muscle development.Development (Cambridge, England) · 2016Article
- LRRC10 is required to maintain cardiac function in response to pressure overload.American journal of physiology. Heart and circulatory physiology · 2016Article
- Mechanosensitive Molecular Networks Involved in Transducing Resistance Exercise-Signals into Muscle Protein Accretion.Frontiers in physiology · 2016Review
- Overexpression of Striated Muscle Activator of Rho Signaling (STARS) Increases C2C12 Skeletal Muscle Cell Differentiation.Frontiers in physiology · 2016Article
- Qiliqiangxin inhibits angiotensin II-induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin-6.Journal of cellular and molecular medicine · 2015Article
Corrections and comments
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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
Cytoskeletal proteins have been implicated in the pathogenesis of cardiomyopathy, but how the cytoskeleton influences the transcriptional alterations associated with adverse cardiac remodeling remains unclear. Striated muscle activator of Rho signaling (STARS) is a muscle-specific actin-binding protein localized to the Z disc that activates serum response factor-dependent (SRF-dependent) transcription by inducing nuclear translocation of the myocardin-related SRF coactivators MRTF-A and -B. We show that STARS expression is upregulated in mouse models of cardiac hypertrophy and in failing human hearts. A conserved region of the STARS promoter containing an essential binding site for myocyte enhancer factor-2 (MEF2), a stress-responsive transcriptional activator, mediates cardiac expression of STARS, which in turn activates SRF target genes. Forced overexpression of STARS in the heart sensitizes the heart to pressure overload and calcineurin signaling, resulting in exaggerated deterioration in cardiac function in response to these hypertrophic stimuli. These findings suggest that STARS modulates the responsiveness of the heart to stress signaling by functioning as a cytoskeletal intermediary between MEF2 and SRF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.