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TAKANO, A. P. C. Inflammation-related aspects in cardiac hypertrophy induced by thyroid hormone. Contribution of the renin-angiotensin system. 2016. 104 p. Ph. D. thesis (Morphological Sciences) – Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, 2016. Recent studies have evidenced the involvement of inflammatory related mechanisms to the development of cardiac hypertrophy and other consequences on cardiovascular system. Previous unpublished results demonstrated increased proinflammatory genes in heart of rats treated with thyroid hormone (TH). In addition, it is well known that the renin-angiotensin system (RAS) induce inflammatory response on cardiovascular system and mediate the cardiac hypertrophy induced by high levels of TH. Based on those evidences, the present study evaluated some aspects related to the inflammatory context in the cardiac hypertrophy induced by TH, and the possible involvement of RAS in this process, by using in vivo and in vitro analysis. The data showed some alterations in circulating and cardiac cytokines from THtreated animals. The expression of calgranulin A (or also known as S100A8) and the myeloid differentiation factor-88 (MyD88) were increased in cardiac tissue of hyperthyroid animals and in cultured cardiomyocytes under T3 stimulation. The contribution of those molecules in the cardiomycyte hypertrophy in response to TH was also demonstrated. Furthermore, S100A8 and MyD88 were crucial mediators of nuclear factor kappa B (NF-қB) activation, which is also fundamental to the hypertrophic growth of TH-treated cardiomyocytes. Finally, the TH action modulating the expression of S100A8 and NF-қB was influenced by RAS, or specifically, by the contribution of angiotensin type 1 receptor (AT1) mediating the TH effects. These data contribute to the knowledge of molecular basis of TH action on cardiac tissue, as well as the crosstalk between TH and RAS, considering the important influence of both endocrine systems to the development of many alterations in the cardiovascular physiopathology.

Fatores relacionados à inflamação na hipertrofia cardíaca induzida pelo hormônio tiroideano. Contribuição do sistema renina-angiotensina.