{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,17]],"date-time":"2026-04-17T04:56:21Z","timestamp":1776401781843,"version":"3.51.2"},"reference-count":35,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2009,11,1]],"date-time":"2009-11-01T00:00:00Z","timestamp":1257033600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2009,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Chagas' disease induced by\n            <jats:italic>Trypanosoma cruzi<\/jats:italic>\n            infection is an important cause of mortality and morbidity affecting the cardiovascular system for which presently available therapies are largely inadequate. We previously reported that transforming growth factor \u03b2 (TGF-\u03b2) is implicated in several regulatory aspects of\n            <jats:italic>T<\/jats:italic>\n            .\n            <jats:italic>cruzi<\/jats:italic>\n            invasion and growth and in host tissue fibrosis. This prompted us to evaluate the therapeutic action of an inhibitor of TGF-\u03b2 signaling (SB-431542) administered during the acute phase of experimental Chagas' disease. Male Swiss mice were infected intraperitoneally with 10\n            <jats:sup>4<\/jats:sup>\n            trypomastigotes of\n            <jats:italic>T<\/jats:italic>\n            .\n            <jats:italic>cruzi<\/jats:italic>\n            (Y strain) and evaluated clinically for the following 30 days. SB-431542 treatment significantly reduced mortality and decreased parasitemia. Electrocardiography showed that SB-431542 treatment was effective in protecting the cardiac conduction system. By 14 day postinfection, enzymatic biomarkers of tissue damage indicated that muscle injury was decreased by SB-431542 treatment, with significantly lower blood levels of aspartate aminotransferase and creatine kinase. In conclusion, inhibition of TGF-\u03b2 signaling in vivo appears to potently decrease\n            <jats:italic>T<\/jats:italic>\n            .\n            <jats:italic>cruzi<\/jats:italic>\n            infection and to prevent heart damage in a preclinical mouse model. This suggests that this class of molecules may represent a new therapeutic agent for acute and chronic Chagas' disease that warrants further clinical exploration.\n          <\/jats:p>","DOI":"10.1128\/aac.00580-09","type":"journal-article","created":{"date-parts":[[2009,9,9]],"date-time":"2009-09-09T02:08:27Z","timestamp":1252462107000},"page":"4694-4701","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":57,"title":["Pharmacological Inhibition of Transforming Growth Factor \u03b2 Signaling Decreases Infection and Prevents Heart Damage in Acute Chagas' Disease"],"prefix":"10.1128","volume":"53","author":[{"given":"Mariana C.","family":"Waghabi","sequence":"first","affiliation":[{"name":"Laborato\u0301rio de Inovac\u0327o\u0303es em Terapias, Ensino e Bioprodutos"},{"name":"Laborato\u0301rio de Geno\u0302mica Funcional e Bioinforma\u0301tica, Instituto Oswaldo Cruz, Av. 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