+ Site Statistics
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Protective Function of STAT3 in CVB3-Induced Myocarditis



Protective Function of STAT3 in CVB3-Induced Myocarditis



Cardiology Research and Practice 2012: 437623



The transcription factor signal transducer and activator of transcription 3 (STAT3) is an important mediator of the inflammatory process. We investigated the role of STAT3 in viral myocarditis and its possible role in the development to dilated cardiomyopathy. We used STAT3-deficent mice with a cardiomyocyte-restricted knockout and induced a viral myocarditis using Coxsackievirus B3 (CVB3) which induced a severe inflammation during the acute phase of the viral myocarditis. A complete virus clearance and an attenuated inflammation were examined in both groups WT and STAT3 KO mice 4 weeks after infection, but the cardiac function in STAT3 KO mice was significantly decreased in contrast to the infected WT mice. Interestingly, an increased expression of collagen I was detected in STAT3 KO mice compared to WT mice 4 weeks after CVB3 infection. Furthermore, the matrix degradation was reduced in STAT3 KO mice which might be an explanation for the observed matrix deposition. Consequently, we here demonstrate the protective function of STAT3 in CVB3-induced myocarditis. Since the cardiomyocyte-restricted knockout leads to an increased fibrosis, it can be assumed that STAT3 signalling in cardiomyocytes protects the heart against increased fibrosis through paracrine effects.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 055244605

Download citation: RISBibTeXText

PMID: 22675647

DOI: 10.1155/2012/437623


Related references

Epitopes shared between coxsackievirus B3 (CVB3) and normal heart tissue contribute to CVB3-induced murine myocarditis. Clinical Immunology and Immunopathology 68(2): 129-134, 1993

The heart-protective mechanism of Qishaowuwei formula on murine viral myocarditis induced by CVB3. Journal of Ethnopharmacology 127(2): 221-228, 2010

The heart-protective mechanism of nitronyl nitroxide radicals on murine viral myocarditis induced by CVB3. Biochimie 94(9): 1951-1959, 2012

Studies on the mechanisms of resistance to coxsackievirus b3 cvb3 induced myocarditis at adolescence in mice vaccinated at birth with a temperature sensitive mutant of cvb3. European Heart Journal 8(Suppl. J): 403-406, 1987

Studies on the mechanism(s) of resistance to coxsackie virus B3 (CVB3)-induced myocarditis at adolescence in mice vaccinated at birth with a temperature-sensitive mutant of CVB3. European Heart Journal 8(Suppl J): 403-405, 1987

IL-22-producing Th22 cells play a protective role in CVB3-induced chronic myocarditis and dilated cardiomyopathy by inhibiting myocardial fibrosis. Virology Journal 11: 230, 2014

Inhibition of coagulation factor Xa improves myocardial function during CVB3-induced myocarditis. Cardiovascular Therapeutics 32(3): 113-119, 2014

Simvastatin's protective effect and its mechanism in acute period of viral myocarditis caused by CVB3 in mice. Wuhan Daxue Xuebao (Yixue Ban) 28(6): 722-725, 2007

TRAF6: A player in CVB3-induced myocarditis?. Cytokine 122: 154143, 2019

Soluble DAF abrogates CVB3-induced myocarditis in mice. International Immunopharmacology 2(9): 1365-1366, 2002

T lymphocyte responses in CVB3-induced murine myocarditis. Scandinavian Journal of Infectious Diseases. Supplementum 88: 67-78, 1993

Genetic regulation of CVB3-induced autoimmune myocarditis. Dissertation Abstracts International B, Sciences and Engineering 49(7): 2485-2486, 1989

A20 (TNFAIP3) alleviates CVB3-induced myocarditis via inhibiting NF-κB signaling. Plos one 7(9): E46515, 2012

Inhibition of 12/15-LO ameliorates CVB3-induced myocarditis by activating Nrf2. Chemico-Biological Interactions 272: 65-71, 2017

MicroRNAs regulate the pathogenesis of CVB3-induced viral myocarditis. Intervirology 56(2): 104-113, 2013