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

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.