{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,31]],"date-time":"2025-12-31T11:10:15Z","timestamp":1767179415649,"version":"build-2238731810"},"update-to":[{"DOI":"10.1371\/journal.pntd.0012703","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2024,12,10]],"date-time":"2024-12-10T00:00:00Z","timestamp":1733788800000}}],"reference-count":75,"publisher":"Public Library of Science (PLoS)","issue":"11","license":[{"start":{"date-parts":[[2024,11,26]],"date-time":"2024-11-26T00:00:00Z","timestamp":1732579200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002322","name":"Coordena\u00e7\u00e3o de Aperfei\u00e7oamento de Pessoal de N\u00edvel Superior","doi-asserted-by":"publisher","award":["Finance Code 001"],"award-info":[{"award-number":["Finance Code 001"]}],"id":[{"id":"10.13039\/501100002322","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","award":["304474\/2015-0, 306037\/2019-0"],"award-info":[{"award-number":["304474\/2015-0, 306037\/2019-0"]}],"id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004586","name":"Funda\u00e7\u00e3o Carlos Chagas Filho de Amparo \u00e0 Pesquisa do Estado do Rio de Janeiro","doi-asserted-by":"publisher","award":["CNE E-26\/ 210.190\/2018, E-26\/202.572\/2019"],"award-info":[{"award-number":["CNE E-26\/ 210.190\/2018, E-26\/202.572\/2019"]}],"id":[{"id":"10.13039\/501100004586","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100006507","name":"Funda\u00e7\u00e3o Oswaldo Cruz","doi-asserted-by":"publisher","award":["PAEF2 and PAEF3"],"award-info":[{"award-number":["PAEF2 and PAEF3"]}],"id":[{"id":"10.13039\/501100006507","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosntds.org"],"crossmark-restriction":false},"short-container-title":["PLoS Negl Trop Dis"],"abstract":"<jats:p>\n                    Chagas disease (CD), a neglected tropical disease, is caused by infection by the protozoan\n                    <jats:italic>Trypanosoma cruzi<\/jats:italic>\n                    . One-third of CD patients develop cardiac disease (CARD), an inflammatory and fibrotic process that may progress to heart failure associated with reduced left ventricular ejection fraction (LVEF). The determinants of CD progression are still uncertain. In non-infectious conditions, the angiotensin-converting enzyme (ACE) functional insertion (I)\/deletion (D) and type 1 angiotensin II receptor (AT\n                    <jats:sub>1<\/jats:sub>\n                    R) +1166A&gt;C gene polymorphisms have been linked to clinical outcomes. In a Brazilian cohort of 402 patients with positive serology for CD, in a case-control study we used PCR for genotyping the\n                    <jats:italic>ACE<\/jats:italic>\n                    rs4646994 I\/D and\n                    <jats:italic>AGTR1<\/jats:italic>\n                    rs5182C&gt;T, rs275653 -119C&gt;T, rs2131127A&gt;G and rs5186 +1166A&gt;C polymorphisms to evaluate association with CARD and progression to heart failure. Patients were classified as non-CARD (stage A; 109), and mild (stage B1; 161) or severe (stage C; 132) CARD. The groups were compared using unconditional logistic regression analysis and adjusted for non-genetic covariates (age, gender, and trypanocidal treatment).\n                    <jats:italic>ACE<\/jats:italic>\n                    II genotype appeared less frequent in C patients (15% in C\n                    <jats:italic>vs<\/jats:italic>\n                    20% in B1 and 27% in A). After covariate adjustments, the\n                    <jats:italic>ACE<\/jats:italic>\n                    D allele showed a borderline association with susceptibility to severe CARD (C\n                    <jats:italic>vs<\/jats:italic>\n                    A: OR = 1.9;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.08).\n                    <jats:italic>AGTR1<\/jats:italic>\n                    +1166AC genotype showed a borderline association with protection against the progression and severity of CARD (C\n                    <jats:italic>vs<\/jats:italic>\n                    A: OR = 0.6;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.09; C\n                    <jats:italic>vs<\/jats:italic>\n                    B1: OR = 0.6;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.07; C\n                    <jats:italic>vs<\/jats:italic>\n                    A + B1: OR = 0.6;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.05). However, adjustments for multiple comparisons showed no association of\n                    <jats:italic>ACE<\/jats:italic>\n                    I\/D and\n                    <jats:italic>AGTR1<\/jats:italic>\n                    polymorphisms with susceptibility and severity of CARD. The rs275653\/rs2131127\/rs5186\/rs5182 T\/A\/C\/T haplotype was protective against progression to the severe form of CARD (C\n                    <jats:italic>vs<\/jats:italic>\n                    B1: OR = 0.3;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.03). Moreover, patients with\n                    <jats:italic>ACE<\/jats:italic>\n                    II and\n                    <jats:italic>AGTR1<\/jats:italic>\n                    rs5186 +1166AC genotypes presented higher LVEF%. In C patients, TNF serum levels were higher in\n                    <jats:italic>ACE<\/jats:italic>\n                    D carriers than in II genotype. Although limited in number, a cross-sectional observation suggests that C-stage patients treated with benznidazole years prior to administration of ACE inhibitors\/AT\n                    <jats:sub>1<\/jats:sub>\n                    R antagonists show reduced TNF serum levels and improved LVEF%. Therefore, variants of\n                    <jats:italic>ACE<\/jats:italic>\n                    and\n                    <jats:italic>AGTR1<\/jats:italic>\n                    genes may influence the outcome of Chagas\u2019 heart disease and should be explored in precision medicine. Further, pharmacotherapies may improve immunological abnormality and clinical outcome in CD patients. Altogether, these data support prospective studies of this cohort and replication in other cohorts.\n                  <\/jats:p>","DOI":"10.1371\/journal.pntd.0012703","type":"journal-article","created":{"date-parts":[[2024,11,26]],"date-time":"2024-11-26T14:06:56Z","timestamp":1732630016000},"page":"e0012703","update-policy":"https:\/\/doi.org\/10.1371\/journal.pntd.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["Influence of angiotensin II type 1 receptors and angiotensin-converting enzyme I\/D gene polymorphisms on the progression of Chagas\u2019 heart disease in a Brazilian cohort: Impact of therapy on clinical outcomes"],"prefix":"10.1371","volume":"18","author":[{"given":"Thayse do Esp\u00edrito Santo","family":"Prot\u00e1sio da Silva","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucia Elena","family":"Alvarado-Arnez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Angelica Martins","family":"Batista","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Silvia Marinho Martins","family":"Alves","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gloria","family":"Melo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cristina Veloso","family":"Carrazzone","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Isabelle de Oliveira","family":"Moraes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonio G.","family":"Pacheco","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Camila","family":"Sarteschi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Milton Oz\u00f3rio","family":"Moraes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wilson","family":"Oliveira Jr","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5503-6754","authenticated-orcid":true,"given":"Joseli","family":"Lannes-Vieira","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"340","published-online":{"date-parts":[[2024,11,26]]},"reference":[{"key":"pntd.0012703.ref001","first-page":"2023","volume":"11","author":"WHO","year":"2023","journal-title":"Chagas disease (also known as American trypanosomiasis) (who.int)."},{"key":"pntd.0012703.ref002","doi-asserted-by":"crossref","first-page":"27","DOI":"10.1007\/978-3-030-44054-1_2","volume-title":"Chagas disease\u2013a neglected tropical disease.","author":"BA de Noya","year":"2020"},{"issue":"3","key":"pntd.0012703.ref003","doi-asserted-by":"crossref","first-page":"164","DOI":"10.1053\/j.semdp.2019.04.008","article-title":"Chagas disease as example of a reemerging parasite.","volume":"36","author":"J. 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