Association between inflammation-related pathways and cardiac hypertrophy induced by thyroid hormone. Role of the Renin-Angiotensin System

• Grant number: 11/23352-4
• Support Opportunities: Scholarships in Brazil - Doctorate
• Start date: April 01, 2012
• End date: April 30, 2016
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Maria Luiza de Morais Barreto de Chaves
• Grantee: Ana Paula Cremasco Takano
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated scholarship(s): 15/01166-5 - Effect of cardiac specific inhibition of NF-kB in cardiac hypertrophy induced by thyroid hormone, BE.EP.DR

Abstract

High levels of thyroid hormones (TH) result in changes in the cardiovascular system including, for example, cardiac hypertrophy, which is experimentally confirmed in vivo and in vitro. Data from our group demonstrated significant participation of the renin-angiotensin system (RAS) in this process and other cardiovascular actions of TH. Although these studies have contributed to the advancement of knowledge about the crosstalk between these two endocrine systems (RAS and TH), the molecular mechanisms related to this process are not yet fully understood. Previous results obtained by our group have also shown that hyperthyroid rat hearts have increased expression of proteins related to inflammation, such as TGF-²1 and calgranulin A and B. Whereas angiotensin II (Ang II), the effector peptide of the RAS, is capable of inducing the inflammatory response in heart tissue and that inhibition of this system leads to prevention of cardiac hypertrophy, our goal is to assess whether the hypertrophy promoted by high levels of TH occurs as a consequence of activation of inflammatory pathways and whether there is any involvement of SRA in the process.

Scientific publications

(The scientific publications listed on this page originate from the Web of Science or SciELO databases. Their authors have cited FAPESP grant or fellowship project numbers awarded to Principal Investigators or Fellowship Recipients, whether or not they are among the authors. This information is collected automatically and retrieved directly from those bibliometric databases.)

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. 12-pg., 2017-06-01. (11/23352-4, 15/01166-5, 13/22480-4)

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. (11/23352-4, 15/01166-5, 13/22480-4)

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. (11/23352-4, 13/22480-4)

Academic Publications

(References retrieved automatically from State of São Paulo Research Institutions)

TAKANO, Ana Paula Cremasco. Inflammation-related aspects in cardiac hypertrophy induced by thyroid hormone. Contribution of the renin-angiotensin system.. 2016. Doctoral Thesis - Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) São Paulo.