Figure 3.

Contrasting roles of STAT3 in viral myocarditis. Cardiac myocyte-specific STAT3 protects against the initiation and development if the dilated phenotype by maintaining expression levels of dystrophin and α-sarcoglycan. Activation of STAT3 by stimulation of the α7nAchR in macrophages alleviates myocarditis by favoring a less inflammatory phenotype. In contrast, STAT3 contributes to myocarditis due to enhanced hepatic and cardiac IL-6 production, as well as IL-6-induced complement component C3 production in the liver. STAT3 also contributes to the differentiation and expansion of Th17 cells that have a role in the development of myocarditis. See text for additional details. Images adapted from Servier Medical Art (https://smart.servier.com/).