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Inflammation and cardiac hypertrophy induced by thyroid hormones: contribution of renin-angiotensin system

Abstract

Elevated levels of Thyroid Hormones promote a series of cardiovascular changes including cardiac hypertrophy, which may be assessed directly by in vitro or in vivo approaches. We and other authors have evidenced in diverse studies a close relationship between the cardiac effects of Thyroid Hormones and Renin-Angiotensin System (RAS) activation. However, some molecular mechanisms involving this endocrine interaction remains to be solved.Recently we have obtained some results demonstrating that hearts from hyperthyroid rats presented increased Calgranulin A and B expression levels, a protein directly involved to inflammatory processes. Based on the Angiotensin II corresponds to the main peptide of RAS and induces an inflammatory response on cardiovascular system and also considering that the RAS inhibition prevents the cardiac hypertrophy induced by Thyroid Hormones our purpose is to evaluate the possible involvement of inflammatory pathways activation in this cardiac hypertrophy model. The role or contribution of RAS will be also evaluated in the present study. (AU)

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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)
CREMASCO TAKANO, ANA PAULA; SENGER, NATHALIA; MUNHOZ, CAROLINA DEMARCHI; MORAIS BARRETO-CHAVES, MARIA LUIZA. AT1 receptor blockage impairs NF-kappa B activation mediated by thyroid hormone in cardiomyocytes. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, v. 470, n. 3, p. 549-558, MAR 2018. Web of Science Citations: 1.
CREMASCO TAKANO, ANA PAULA; MUNHOZ, CAROLINA DEMARCHI; MORISCOT, ANSELMO SIGARI; GUPTA, SUDHIRANJAN; MORAIS BARRETO-CHAVES, MARIA LUIZA. S100A8/MYD88/NF-O > B: a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone. JOURNAL OF MOLECULAR MEDICINE-JMM, v. 95, n. 6, p. 671-682, JUN 2017. Web of Science Citations: 4.

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