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AT1R internalization and Ras/Raf/MEK/ERK signaling in the cardiomyocyte hypertrophy induced by thyroid hormone. role of beta-arrestins

Abstract

Thyroid Hormones (TH) exert numerous effects in the cardiovascular system.In this way, the hyperthyroidism is associated to elevated cardiac function and morphologic alterations in the heart as cardiac hypertrophy. We have described that the increase of cardiac mass induced by TH is mediated, at least in part by activation of Renin-Angiotensin System, mainly by AT1 Receptor (AT1R). This receptor when activated may stimulate two different mechanims of signaling: mechanism G- protein dependent or G-protein independent, mediated by beta-arrestins. Herein we will evaluate the contribution of beta-arrestins and Raf/MEK/ERK pathway signaling in the cardiomyocyte hypertrophy indeced by TH. (AU)

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
SENGER, NATHALIA; C. PARLETTA, ALINE; MARQUES, BRUNO V. D.; AKAMINE, ELIANA H.; DINIZ, GABRIELA P.; CAMPAGNOLE-SANTOS, MARIA J.; SANTOS, ROBSON A. S.; BARRETO-CHAVES, MARIA LUIZA M. Angiotensin-(1-7) prevents T3-induced cardiomyocyte hypertrophy by upregulating FOXO3/SOD1/catalase and downregulating NF-x138;B. Journal of Cellular Physiology, v. 236, n. 4, p. 3059-3072, APR 2021. Web of Science Citations: 1.
LINO, CAROLINE ANTUNES; DE BORTOLI TEIXEIRA, LARISSA; CAPELUPE SIMOES, SARAH; DE OLIVEIRA SILVA, TABATHA; DINIZ, GABRIELA PLACONA; DA COSTA-NETO, CLAUDIO MIGUEL; BARRETO-CHAVES, MARIA LUIZA MORAIS. Beta-arrestin 2 mediates cardiac hypertrophy induced by thyroid hormones via AT1R. Journal of Cellular Physiology, v. 236, n. 6 DEC 2020. Web of Science Citations: 0.
BARRETO-CHAVES, M. L. M.; SENGER, N.; FEVEREIRO, M. R.; PARLETTA, A. C.; TAKANO, A. P. C. Impact of hyperthyroidism on cardiac hypertrophy. ENDOCRINE CONNECTIONS, v. 9, n. 3, p. R59-R69, MAR 2020. Web of Science Citations: 0.

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