Immunomodulation by atorvastatin upregulates expression of gap junction proteins in coxsackievirus B3 (CVB3)-induced myocarditis

Abstract

This study shows for the first time that myocardial expression of Cxs is downregulated during CVB3-induced myocarditis and that immunomodulation by atorvastatin could restore the impaired gap junction channels and improve the outcome of viral myocarditis.

Study of Atorvastatin in experimental allergic airway inflammation in mice

“…IL-10 has been demonstrated to be essential for the presence of airway hyperresponsiveness but not essential for the pulmonary inflammation [8]. The effect of Atorvastatin on these cytokines would be explained in the view of studying its effects on Th1 cytokine, for better understanding of its possible immune modulatory effects in allergy as shown in previous studies [26,27].…”

Statins as Anti-Inflammatory Agents in Atherogenesis: Molecular Mechanisms and Lessons from the Recent Clinical Trials

“…In a murine model of viral myocarditis, atorvastatin decreased myocardial TNF-α and IFN-γ and increased connexins expression, resulting in improved survival [87]. Other experimental studies suggest that pre-treatment with simvastatin significantly reduced systemic and myocardial levels of pro-inflammatory cytokines post cardiopulmonary bypass by stimulating PPAR-γ receptors and inhibiting NF-κB expression in myocardial tissue [31].…”

Statins as a New Therapeutic Perspective in Myocarditis and Postmyocarditis Dilated Cardiomyopathy

“…On the basis of the above data and in consideration of the key role played by T helper cells in the pathogenesis of myocarditis, in the last years several authors [16][17][18][19][20][21][22][23][24] investigated the therapeutic potential as well as the putative underlying mechanisms of statin administration in animal models of the disease ( Table 1). The results of these studies, in which different molecules were used (mainly atorvastatin, but also fluvastatin, simvastatin, rosuvastatin and pitavastatin), clearly and consistently demonstrated the ability of this class of drugs to significantly improve both cardiac function, as assessed by echocardiography, and the histopathological severity of the disease, with respect to untreated animals.…”

“…In turn, these effects finally result in a marked reduction of the amount of cardiac Th1-type and proinflammatory cytokines, thus attenuating their harmful consequences on the myocardium, i.e. cardiomyocyte apoptosis, and structural and electrophysiological remodelling, which are chiefly involved in the severe depression of cardiac function, and the high arrhythmic risk characterizing myocarditis and inflammatory DCM [16][17][18][19][20][21][22][23][24].…”