ArticleMolecular and cellular biochemistry2003
Cardiotrophin-1: expression in experimental myocardial infarction and potential role in post-MI wound healing.
Article in Molecular and cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 72 citations in OpenAlex.
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- From dissection of fibrotic pathways to assessment of drug interactions to reduce cardiac fibrosis and heart failure.Current research in pharmacology and drug discovery · 2021Review
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- Developmental stage-dependent effects of cardiac fibroblasts on function of stem cell-derived engineered cardiac tissues.Scientific reports · 2017Article
- Cardiotrophin-1 promotes cardiomyocyte differentiation from mouse induced pluripotent stem cells via JAK2/STAT3/Pim-1 signaling pathway.Journal of geriatric cardiology : JGC · 2015Article
- Modulation of cardiac fibrosis by Krüppel-like factor 6 through transcriptional control of thrombospondin 4 in cardiomyocytes.Cardiovascular research · 2015Article
- Interleukin-6 signaling, soluble glycoprotein 130, and inflammation in heart failure.Current heart failure reports · 2014Review
- Fasudil, a Rho-kinase inhibitor, protects against excessive endurance exercise training-induced cardiac hypertrophy, apoptosis and fibrosis in rats.European journal of applied physiology · 2012Article
- Cellular Interplay between Cardiomyocytes and Nonmyocytes in Cardiac Remodeling.International journal of inflammation · 2011Article
- Cardiotrophin-1 maintains the undifferentiated state in skeletal myoblasts.The Journal of biological chemistry · 2009Article
- Biological functions of the low and high molecular weight protein isoforms of fibroblast growth factor-2 in cardiovascular development and disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Review
- The immune system and cardiac repair.Pharmacological research · 2008Review
- Changes of collagen metabolism predict the left ventricular remodeling after myocardial infarction.Molecular and cellular biochemistry · 2006Article
- Article
- Differential gene expression in infarct scar and viable myocardium from rat heart following coronary ligation.Journal of cellular and molecular medicineArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiotrophin-1 (CT-1), a member of the IL-6 family of cytokines, has been shown to be elevated in the serum of patients with ischemic heart disease and valvular heart disease, and induces cardiomyocyte hypertrophy in vitro. We investigated expression of CT-1 in post-MI rat heart and the effect of CT-1 on cultured primary adult rat cardiac fibroblasts. Elevated CT-1 expression was observed in the infarct zone at 24 h and continued through 2, 4 and 8 weeks post-MI, compared to sham-operated animals. CT-1 induced rapid phosphorylation of Jak, Jak2, STAT1, STAT3, p42/44 MAPK and Akt in cultured adult cardiac fibroblasts. CT-1 induced cardiac fibroblast protein synthesis and proliferation. Protein and DNA synthesis were dependent on activation of Jak/STAT, MEK1/2, PI3K and Src pathways as evidenced by decreased 3H-leucine and 3H-thymidine incorporation after pretreatment with AG490, PD98059, LY294002 and genistein respectively. Furthermore, CT-1 treatment increased procollagen-1-carboxypropeptide (PICP) synthesis, a marker of mature collagen synthesis. CT-1 induced cell migration of rat cardiac fibroblasts. Our results suggest that CT-1, as expressed in post-MI heart, may play an important role in infarct scar formation and ongoing remodeling of the scar. CT-1 was able to initiate each of the processes considered important in the formation of infarct scar including cardiac fibroblast migration as well as fibroblast proliferation and collagen synthesis. Further work is required to determine factors that induce CT-1 expression and interplay with other mediators of cardiac infarct wound healing in the setting of acute cardiac ischemia and chronic post-MI heart failure.
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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.