CV Lattes
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Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB) (Institutional affiliation for the last research proposal) Birthplace: Portugal
graduation at Abi - Ciências Biológicas from Universidade de São Paulo (1990) and doctorate at Physiology from Universidade de São Paulo (1996). He is currently associated professor at Universidade de São Paulo. Has experience in Morphology, focusing on Morphology, acting on the following subjects: hormônios tiroideanos, sistema renina-angiotensina, hipertrofia cardíaca, enzima conversora de angiotensina i and angiotensin-converting enzyme. (Source: Lattes Curriculum)
Cardiovascular diseases remain the leading cause of global morbidity and mortality today. Even considering the scientific and technological advances of the last two decades, it is estimated that in 2030 more than 23 million people will die due to cardiovascular diseases. Although different stimuli may induce heart failure (HF), it is preceded by cardiac hypertrophy, characterized by incre…
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 r…
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…
Several endocrine systems, such as the renin-angiotensin system (RAS) and thyroid hormones (TH) alter the cardiac function, directly or indirectly modulating the heart trophism and protecting against cardiac stress. Besides their regulatory role under situations of cardiac damage, the endocrine systems are able to interact in many of their actions. The TH promote a phenotype of cardioprot…
(Only some records are available in English at this moment)
We have previously demonstrated that T3 induces to increased S100A8 levels, a DAMP involved with TLR4/MyD88/NF-kB signaling and important to cardiac hypertrophy observed in hyperthyroidism. This signaling pathway is critical to activation of intracellular sensors as NLRP3, AIM2, NLRC4 and inlammasome activation. On the other hand, beta-adrenergic stimulation also acts in the NF-kB signali…
Cardiac hypertrophy, despite being an adaptive response may contribute to cardiomyopathy development and progression. It is well established that thyroid hormones exert direct and indirect effects on the heart, which result on an hypertrophic state of this organ. In this sense, our research group has been studying the various cellular and molecular mechanisms involved in this process. Rec…
High levels of thyroid hormones (TH) are responsible for promoting changes in the cardiovascular system, which culminate in the development of cardiac arrhythmias and the installation of a hypertrophic process (Cappola et al., 2006). We have previously demonstrated that TH is able to promote cardiac hypertrophy and other cardiovascular manifestations through Renin-Angiotensin-System (RAS)…
In order to better understand the previously described interaction between the renin angiotensin system (RAS), specifically the angiotensin II receptor type 1 (AT1R), and the effects of thyroid hormone (T3) administration in cardiac muscle cells, this study proposes the analysis of receptor internalization - an important mechanism of signal transduction regulation. The ²-arrestins (²ARRs)…
(Only some records are available in English at this moment)
Although most of effects of nuclear factor kappaB (NF-kB) is related to inflammatoryresponse, this nuclear factor has been shown to be involved in the development ofcardiac hypertrophy resulted by diverse stimuli. In the present study, we willinvestigate whether the thyroid hormone (TH) action leading to cardiac hypertrophy ismediated by NF-kB. Transgenic mice that contain specific mut…
The heart corresponds to main target of TH and many of the classic signs and symptoms of hyperthyroidism are the cardiac and hemodynamic manifestations which include heart rhythm disorders. The present study has as aim to define the role of Caveolin-1 (Cav-1) depletion and oxidative stress in the pro-arrhythmic effects of hyperthyroidism. We will define whether Cav-1 deletion in mice lead…
| 1 / 1 | Ongoing research grants |
| 12 / 6 | Completed research grants |
| 1 / 1 | Ongoing scholarships in Brazil |
| 33 / 15 | Completed scholarships in Brazil |
| 2 / 2 | Completed scholarships abroad |
| 49 / 25 | All research grants and scholarships |
| Associated processes | |
(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)
| Publications | 15 |
| Citations | 86 |
| Cit./Article | 5.7 |
| Data from Web of Science | |
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. (16/13896-0, 13/16142-9)
LINO, CAROLINE ANTUNES; DEMASI, MARILENE; BARRETO-CHAVES, MARIA LUIZA. Ubiquitin proteasome system (UPS) activation in the cardiac hypertrophy of hyperthyroidism. Molecular and Cellular Endocrinology, v. 493, AUG 1 2019. Web of Science Citations: 1. (11/01291-3)
CARNEIRO-RAMOS, M. S.; DINIZ, G. P.; NADU, A. P.; ALMEIDA, J.; VIEIRA, R. L. P.; SANTOS, R. A. S.; BARRETO-CHAVES, M. L. M.. Blockage of Angiotensin II type 2 receptor prevents thyroxine-mediated cardiac hypertrophy by blocking Akt activation. BASIC RESEARCH IN CARDIOLOGY, v. 105, n. 3, p. 325-335, MAY 2010. Web of Science Citations: 29.
CARRILLO-SEPULVEDA, MARIA ALICIA; CERAVOLO, GRAZIELA S.; FURSTENAU, CRISTINA R.; MONTEIRO, PRISCILLA DE SOUZA; BRUNO-FORTES, ZULEICA; CARVALHO, MARIA HELENA; LAURINDO, FRANCISCO R.; TOSTES, RITA C.; WEBB, R. CLINTON; BARRETO-CHAVES, MARIA LUIZA M.. Emerging Role of Angiotensin Type 2 Receptor (AT2R)/Akt/NO Pathway in Vascular Smooth Muscle Cell in the Hyperthyroidism. PLoS One, v. 8, n. 4, APR 24 2013. Web of Science Citations: 15. (06/61523-7)
M.L.M. BARRETO-CHAVES; A. HEIMANN; J.E. KRIEGER. Stimulatory effect of dexamethasone on angiotensin-converting enzyme in neonatal rat cardiac myocytes. Brazilian Journal of Medical and Biological Research, v. 33, n. 6, p. 661-664, Jun. 2000.
CHIASSON, VALORIE; TAKANO, ANA PAULA CREMASCO; GULERIA, RAKESHWAR S.; GUPTA, SUDHIRANJAN. Deficiency of MicroRNA miR-1954 Promotes Cardiac Remodeling and Fibrosis. JOURNAL OF THE AMERICAN HEART ASSOCIATION, v. 8, n. 21, NOV 5 2019. Web of Science Citations: 0. (15/01166-5)
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. (16/13896-0)
CREMASCO TAKANO, ANA PAULA; DINIZ, GABRIELA PLACONA; MORAIS BARRETO-CHAVES, MARIA LUIZA. AMPK signaling pathway is rapidly activated by T3 and regulates the cardiomyocyte growth. Molecular and Cellular Endocrinology, v. 376, n. 1-2, p. 43-50, AUG 25 2013. Web of Science Citations: 8. (09/16888-5, 09/09922-2)
CARNEIRO-RAMOS‚ MS; SILVA‚ VB; SANTOS‚ RAS; BARRETO-CHAVES‚ MLM. Tissue-specific modulation of angiotensin-converting enzyme (ACE) in hyperthyroidism. Peptides, v. 27, n. 11, p. 2942-2949, 2006.
SENGER, NATHALIA; MELO, MARCOS BARROUIN; DINIZ, GABRIELA PLACONA; CAMPAGNOLE-SANTOS, MARIA JOSE; SOUZA SANTOS, ROBSON AUGUSTO; BARRETO-CHAVES, MARIA LUIZA M.. Angiotensin-(1-7) reduces cardiac effects of thyroid hormone by GSK3 beta/NFATc3 signaling pathway. Clinical Science, v. 132, n. 11, p. 1117-1133, JUN 14 2018. Web of Science Citations: 1. (13/16348-6)
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. (16/13896-0)
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. (11/23352-4, 13/22480-4)
DINIZ, GABRIELA PLACONA; LINO, CAROLINE ANTUNES; MORENO, CAMILA RODRIGUES; SENGER, NATHALIA; MORAIS BARRETO-CHAVES, MARIA LUIZA. MicroRNA-1 overexpression blunts cardiomyocyte hypertrophy elicited by thyroid hormone. Journal of Cellular Physiology, v. 232, n. 12, p. 3360-3368, DEC 2017. Web of Science Citations: 6. (09/14567-7)
DINIZ, GABRIELA PLACONA; LINO, CAROLINE ANTUNES; GUEDES, ELAINE CASTILHO; MOREIRA, LUANA DO NASCIMENTO; MORAIS BARRETO-CHAVES, MARIA LUIZA. Cardiac microRNA-133 is down-regulated in thyroid hormone-mediated cardiac hypertrophy partially via Type 1 Angiotensin II receptor. BASIC RESEARCH IN CARDIOLOGY, v. 110, n. 5, SEP 2015. Web of Science Citations: 18. (09/14567-7)
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. (11/23352-4, 15/01166-5, 13/22480-4)
DA SILVA, IVSON BEZERRA; GOMES, DAYANE APARECIDA; ALENINA, NATALIA; BADER, MICHAEL; DOS SANTOS, ROBSON AUGUSTO; BARRETO-CHAVES, MARIA LUIZA M.. Cardioprotective effect of thyroid hormone is mediated by AT2 receptor and involves nitric oxide production via Akt activation in mice. HEART AND VESSELS, v. 33, n. 6, p. 671-681, JUN 2018. Web of Science Citations: 2. (11/12893-4, 13/04703-6)
MCCAULEY, MARK D.; HONG, LIANG; SRIDHAR, ARVIND; MENON, AMBILI; PERIKE, SRIKANTH; ZHANG, MEIHONG; DA SILVA, IVSON BEZERRA; YAN, JIAJIE; BONINI, MARCELO G.; AI, XUN; et al. Ion Channel and Structural Remodeling in Obesity-Mediated Atrial Fibrillation. CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY, v. 13, n. 8, AUG 2020. Web of Science Citations: 0. (14/21464-8)
(References retrieved automatically from State of São Paulo Research Institutions)
LINO, Caroline Antunes. Contribuição da sinalização dependente de beta-arrestinas, via receptor de angiotensina II do tipo 1, na hipertrofia cardiomiocítica induzida por T3.. Tese (Doutorado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (13/16142-9)
SHIBATA, Caroline Emy Rodrigues. Efeito do hipertiroidismo experimental, induzido em ratas durante a gestação, sobre componentes do sistema renina-angiotensina cardíaco da prole.. Dissertação (Mestrado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (09/02923-3)
MONTEIRO, Priscilla de Souza. O efeito do hipotiroidismo experimental sobre os componentes da matriz extracelular de aortas torácicas de ratos.. Dissertação (Mestrado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (10/00934-5)
LINO, Caroline Antunes. O sistema ubiquitina-proteassoma no modelo de hipertrofia cardíaca induzida por hormônio tireoidiano.. Dissertação (Mestrado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (11/01291-3)
SEPULVEDA, Maria Alicia Carrillo. Participação do receptor AT2 da angiotensina II no relaxamento vascular promovido pelo hormônio tiroideano. Tese (Doutorado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (06/54064-6)
DINIZ, Gabriela Placoná. Avaliação da contribuição do receptor AT1 de angiotensina II e do papel da via de sinalização AKT/GSK-3/mTOR no processo de hipertrofia do cardiomiócito induzido pelo hormônio tiroideano. Tese (Doutorado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (05/58998-0)
TAKANO, Ana Paula Cremasco. Análise do papel da proteína quinase ativada pela AMP (AMPK) na hipertrofia do cardiomiócito induzida pelo hormônio tiroideano.. Dissertação (Mestrado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (09/09922-2)
TAVARES, Felix Meira. Efeito do hormônio tiroideano na função cardíaca no modelo de isquemia/reperfusão em ratos. Papel do receptor AT2 e da via intracelular AMPK.. Dissertação (Mestrado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (10/00933-9)
TAKANO, Ana Paula Cremasco. Fatores relacionados à inflamação na hipertrofia cardíaca induzida pelo hormônio tiroideano. Contribuição do sistema renina-angiotensina.. Tese (Doutorado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (11/23352-4)
SILVA, Ivson Bezerra da. Efeito cardioprotetor do hormônio tireoidiano no modelo de isquemia/reperfusão: participação do sistema renina-angiotensina.. Tese (Doutorado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (13/04703-6)
TAKANO, Ana Paula Cremasco. Fatores relacionados à inflamação na hipertrofia cardíaca induzida pelo hormônio tiroideano. Contribuição do sistema renina-angiotensina.. Tese (Doutorado) - Instituto de Ciências Biomédicas. Universidade de São Paulo (USP). São Paulo. (11/23352-4)