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. 2021 Aug 24;11:708325. doi: 10.3389/fcimb.2021.708325

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Copyright © 2021 Hoffman, Villar, Poveda, Bottazzi, Hotez, Tweardy and Jones

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Signal transducer and activator of transcription-3 (STAT3) modulation of the cardiac inflammatory–fibrotic axis in chronic Chagasic cardiomyopathy (CCC). Depicted is the cardiac pathology continuum that starts in the acute phase with a predominantly inflammatory response in the heart, which develops into a predominantly fibrotic response in the heart with progression into chronic disease. The role of STAT3 and its upstream and downstream signaling mediators is also depicted. In our model of CCC, STAT3 was found to promote fibrosis via transforming growth factor beta (TGF-β) and platelet-derived growth factor (PDGF) signaling while suppressing inflammatory signaling that involved interferon-γ (IFN-γ) and interleukin-6 (IL-6). Upon inhibition of STAT3, inflammation increased and fibrosis decreased in the heart. The image was created with the assistance of BioRender.