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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Angiotensin-(1-7) prevents T3-induced cardiomyocyte hypertrophy by upregulating FOXO3/SOD1/catalase and downregulating NF-x138;B

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Author(s):
Senger, Nathalia [1] ; C. Parletta, Aline [1] ; Marques, Bruno V. D. [2] ; Akamine, Eliana H. [2] ; Diniz, Gabriela P. [1] ; Campagnole-Santos, Maria J. [3] ; Santos, Robson A. S. [3] ; Barreto-Chaves, Maria Luiza M. [1]
Total Authors: 8
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, Sao Paulo - Brazil
[3] Univ Fed Minas Gerais, Inst Biol Sci, Dept Physiol & Biophys, Belo Horizonte, MG - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Journal of Cellular Physiology; v. 236, n. 4, p. 3059-3072, APR 2021.
Web of Science Citations: 1
Abstract

Clinical studies have shown a correlation between thyroid disorders and cardiac diseases. High levels of triiodothyronine (T3) induce cardiac hypertrophy, a risk factor for cardiac complications and heart failure. Previous results have demonstrated that angiotensin-(1-7) is able to block T3-induced cardiac hypertrophy; however, the molecular mechanisms involved in this event have not been fully elucidated. Here, we evidenced the contribution of FOXO3 signaling to angiotensin-(1-7) effects. Angiotensin-(1-7) treatment increased nuclear FOXO3 levels and reduced p-FOXO3 levels (inactive form) in isolated cardiomyocytes. Knockdown of FOXO3 by RNA silencing abrogated the antihypertrophic effect of angiotensin-(1-7). Increased expression of antioxidant enzymes superoxide dismutase 1 (SOD1 and catalase) and lower levels of reactive oxygen species and nuclear factor-kappa B (NF-kappa B) were observed after angiotensin-(1-7) treatment in vitro. Consistent with these results, transgenic rats overexpressing angiotensin-(1-7) displayed increased nuclear FOXO3 and SOD1 levels and reduced NF-kappa B levels in the heart. These results provide a new molecular mechanism responsible for the antihypertrophic effect of angiotensin-(1-7), which may contribute to future therapeutic targets. (AU)

FAPESP's process: 16/13896-0 - AT1R internalization and Ras/Raf/MEK/ERK signaling in the cardiomyocyte hypertrophy induced by thyroid hormone. role of beta-arrestins
Grantee:Maria Luiza de Morais Barreto de Chaves
Support Opportunities: Regular Research Grants