ArticleDisease models & mechanisms2012
Locally expressed IGF1 propeptide improves mouse heart function in induced dilated cardiomyopathy by blocking myocardial fibrosis and SRF-dependent CTGF induction.
Article in Disease models & mechanisms, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
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- Interrelation between α-Cardiac Actin Treadmilling and Myocardin-Related Transcription Factor-A Nuclear Shuttling in Cardiomyocytes.International journal of molecular sciences · 2022Article
- SRF: a seriously responsible factor in cardiac development and disease.Journal of biomedical science · 2022Review
- Late Health Effects of Partial Body Irradiation Injury in a Minipig Model Are Associated with Changes in Systemic and Cardiac IGF-1 Signaling.International journal of molecular sciences · 2021Article
- Antiapoptosis and Antifibrosis Effects ofBioMed research international · 2019Article
- Identification of target genes in cardiomyopathy with fibrosis and cardiac remodeling.Journal of biomedical science · 2018Article
- Nicotinamide Riboside Preserves Cardiac Function in a Mouse Model of Dilated Cardiomyopathy.Circulation · 2018Article
- Review
- Fetal origins of adult cardiac disease: a novel approach to prevent fetal growth restriction induced cardiac dysfunction using insulin like growth factor.Pediatric research · 2017Article
- Identification of the molecular mechanisms underlying dilated cardiomyopathy via bioinformatic analysis of gene expression profiles.Experimental and therapeutic medicine · 2017Article
- Involvement of microRNA-133 and -29 in cardiac disturbances in diabetic ovariectomized rats.Iranian journal of basic medical sciences · 2016Article
- Regulation of Connective Tissue Growth Factor and Cardiac Fibrosis by an SRF/MicroRNA-133a Axis.PloS one · 2015Article
- Dasatinib Attenuates Pressure Overload Induced Cardiac Fibrosis in a Murine Transverse Aortic Constriction Model.PloS one · 2015Article
- The alternative heart: impact of alternative splicing in heart disease.Journal of cardiovascular translational research · 2013Review
- Cardiac fibrosis in mice expressing an inducible myocardial-specific Cre driver.Disease models & mechanisms · 2013Article
- An integrative computational analysis provides evidence for FBN1-associated network deregulation in trisomy 21.Biology open · 2013Article
- Cross talk between cardiac myocytes and fibroblasts: from multiscale investigative approaches to mechanisms and functional consequences.American journal of physiology. Heart and circulatory physiology · 2012Review
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Cardiac fibrosis is critically involved in the adverse remodeling accompanying dilated cardiomyopathies (DCMs), which leads to cardiac dysfunction and heart failure (HF). Connective tissue growth factor (CTGF), a profibrotic cytokine, plays a key role in this deleterious process. Some beneficial effects of IGF1 on cardiomyopathy have been described, but its potential role in improving DCM is less well characterized. We investigated the consequences of expressing a cardiac-specific transgene encoding locally acting IGF1 propeptide (muscle-produced IGF1; mIGF1) on disease progression in a mouse model of DCM [cardiac-specific and inducible serum response factor (SRF) gene disruption] that mimics some forms of human DCM. Cardiac-specific mIGF1 expression substantially extended the lifespan of SRF mutant mice, markedly improved cardiac functions, and delayed both DCM and HF. These protective effects were accompanied by an overall improvement in cardiomyocyte architecture and a massive reduction of myocardial fibrosis with a concomitant amelioration of inflammation. At least some of the beneficial effects of mIGF1 transgene expression were due to mIGF1 counteracting the strong increase in CTGF expression within cardiomyocytes caused by SRF deficiency, resulting in the blockade of fibroblast proliferation and related myocardial fibrosis. These findings demonstrate that SRF plays a key role in the modulation of cardiac fibrosis through repression of cardiomyocyte CTGF expression in a paracrine fashion. They also explain how impaired SRF function observed in human HF promotes fibrosis and adverse cardiac remodeling. Locally acting mIGF1 efficiently protects the myocardium from these adverse processes, and might thus represent a therapeutic avenue to counter DCM.
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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.