» Articles » PMID: 22675647

Protective Function of STAT3 in CVB3-Induced Myocarditis

Overview
Publisher Wiley
Date 2012 Jun 8
PMID 22675647
Citations 12
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

STAT3 Increases CVB3 Replication and Acute Pancreatitis and Myocarditis Pathology via Impeding Nuclear Translocation of STAT1 and Interferon-Stimulated Gene Expression.

Liang T, Zhang Z, Bai Z, Xu L, Xu W Int J Mol Sci. 2024; 25(16).

PMID: 39201692 PMC: 11354559. DOI: 10.3390/ijms25169007.


GPR15-mediated T cell recruitment during acute viral myocarditis facilitated virus elimination and improved outcome.

Stoffers B, Wolf H, Bacmeister L, Kupsch S, Vico T, Marchini T Nat Cardiovasc Res. 2024; 3(1):76-93.

PMID: 39195892 PMC: 11357984. DOI: 10.1038/s44161-023-00401-z.


Dapagliflozin Alleviates Coxsackievirus B3-induced Acute Viral Myocarditis by Regulating the Macrophage Polarization Through Stat3-related Pathways.

Yan P, Song X, Tran J, Zhou R, Cao X, Zhao G Inflammation. 2022; 45(5):2078-2090.

PMID: 35676606 PMC: 9499897. DOI: 10.1007/s10753-022-01677-2.


Signal Transducer and Activator of Transcription-3 Modulation of Cardiac Pathology in Chronic Chagasic Cardiomyopathy.

Hoffman K, Villar M, Poveda C, Bottazzi M, Hotez P, Tweardy D Front Cell Infect Microbiol. 2021; 11:708325.

PMID: 34504808 PMC: 8421853. DOI: 10.3389/fcimb.2021.708325.


Increased prostaglandin-D2 in male STAT3-deficient hearts shifts cardiac progenitor cells from endothelial to white adipocyte differentiation.

Stelling E, Ricke-Hoch M, Erschow S, Hoffmann S, Bergmann A, Heimerl M PLoS Biol. 2020; 18(12):e3000739.

PMID: 33370269 PMC: 7793290. DOI: 10.1371/journal.pbio.3000739.


References
1.
Hilfiker-Kleiner D, Hilfiker A, Drexler H . Many good reasons to have STAT3 in the heart. Pharmacol Ther. 2005; 107(1):131-7. DOI: 10.1016/j.pharmthera.2005.02.003. View

2.
Hilfiker-Kleiner D, Hilfiker A, Fuchs M, Kaminski K, Schaefer A, Schieffer B . Signal transducer and activator of transcription 3 is required for myocardial capillary growth, control of interstitial matrix deposition, and heart protection from ischemic injury. Circ Res. 2004; 95(2):187-95. DOI: 10.1161/01.RES.0000134921.50377.61. View

3.
Hishinuma S, Funamoto M, Fujio Y, Kunisada K . Hypoxic stress induces cardiotrophin-1 expression in cardiac myocytes. Biochem Biophys Res Commun. 1999; 264(2):436-40. DOI: 10.1006/bbrc.1999.1535. View

4.
Pan J, Fukuda K, Kodama H, Makino S, Takahashi T, Sano M . Role of angiotensin II in activation of the JAK/STAT pathway induced by acute pressure overload in the rat heart. Circ Res. 1997; 81(4):611-7. DOI: 10.1161/01.res.81.4.611. View

5.
Tsutamoto T, Hisanaga T, Wada A, Maeda K, Ohnishi M, Fukai D . Interleukin-6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin-6 is an important prognostic predictor in patients with congestive heart failure. J Am Coll Cardiol. 1998; 31(2):391-8. DOI: 10.1016/s0735-1097(97)00494-4. View