| Regulation of inflammation and myocardial fibrosis in experimental autoimmune myocarditis. | |
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MedLine Citation:
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PMID: 21495969 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autoimmune responses and inflammation are involved in the pathogenesis of many cardiovascular diseases. There is compelling evidence that inflammatory mechanisms may contribute to progressive heart failure. Thus, myocardial infiltration of lymphocytes and mononuclear cells, increased expression of pro-inflammatory chemokines and cytokines and circulating autoantibodies are frequently observed in myocarditis and dilated cardiomyopathy (DCM). Experimental autoimmune myocarditis (EAM) in rodents may be elicited by immunization of cardiac myosin and EAM in rats mimics human fulminant myocarditis in the acute phase and human DCM in the chronic phase. Our animal model, EAM was demonstrated to progress into the clinicopathological state similar to DCM in the chronic phase, and was found to be characterized by the enlargement of the heart, dilatation of ventricles, diffuse and extensive myocardial fibrosis, besides being a cellular immunity and inflammation mediated disease. Severity of myocarditis was characterized by increased inflammation, cardiac fibrosis and decreased myocardial performance in rats with DCM. Pharmacological interventions such as angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs) significantly attenuated the myosin-induced inflammation and cardiac fibrosis and thereby improving myocardial function in rats with DCM. A growing body of evidence shows that ACEI and ARBs contribute to the pharmaceutical management of patients with heart failure mediated by immune and inflammatory response. The purpose of this review is to emphasize the role of inflammation and myocardial fibrosis in rats with DCM after EAM and study the effects of pharmacological interventions such as ACEI, ARBs in the treatment of heart failure through the suppression of inflammatory cytokines and fibrosis. |
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Authors:
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Kenichi Watanabe; Vijayakumar Sukumaran; Punniyakoti T Veeraveedu; Rajarajan A Thandavarayan; Narasimman Gurusamy; Meilei Ma; Wawaimuli Arozal; Flori R Sari; Arun Prasath Lakshmanan; Somasundaram Arumugam; Vivian Soetikno; Varatharajan Rajavel; Kenji Suzuki |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Inflammation & allergy drug targets Volume: 10 ISSN: 2212-4055 ISO Abbreviation: Inflamm Allergy Drug Targets Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-03 Completed Date: 2011-09-08 Revised Date: 2011-11-10 |
Medline Journal Info:
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Nlm Unique ID: 101266886 Medline TA: Inflamm Allergy Drug Targets Country: United Arab Emirates |
Other Details:
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Languages: eng Pagination: 218-25 Citation Subset: IM |
Affiliation:
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Department of Clinical, Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharmacy and Applied Life Sciences, 265-1 Higashizima, Niigata City 956-8603, Japan. watanabe@nupals.ac.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin Receptor Antagonists
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pharmacology,
therapeutic use Angiotensin-Converting Enzyme Inhibitors / pharmacology, therapeutic use Animals Autoantigens / administration & dosage, immunology* Autoimmune Diseases / chemically induced, drug therapy, immunology*, physiopathology Cardiac Myosins / administration & dosage, immunology* Fibrosis Humans Inflammation Mice Models, Animal Myocarditis / chemically induced, drug therapy, immunology*, physiopathology Myocardium / immunology* Organ Specificity Rats |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin Receptor Antagonists; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Autoantigens; EC 3.6.1.-/Cardiac Myosins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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