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Role of ACE I/D gene polymorphism on renin angiotensin system and cardiac hypertrophy markers in the heart of diabetic mice.

Grant number: 12/22283-1
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): June 01, 2013
Effective date (End): February 28, 2015
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Tatiana de Sousa da Cunha Uchiyama
Grantee:Roseli Peres Moreira Silvério
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

In the last decades, Diabetes Mellitus (DM) is exponentially growing and much attention has been given to morbidities correlated to this disease, such as cardiovascular complications (CVD). Furthermore, another form of myocardium disease in diabetic patients could be developed without blood pressure alterations or coronary disease directly correlated, such as diabetic cardiomyopathy (DCMP). This complication could lead to myocardium functional and structural alterations that could implicate in pathologic left ventricular hypertrophy (LVH) and systolic dysfunction. Besides increasing cardiomyocyte size, the LVH is also characterized by genes reprogramming as atrial natriuretic peptide (ANP), skeletal ±-actin, ±-myosin heavy chain (±-MHC) and ²-myosin heavy chain (²-MHC), which modulate cardiac contraction. In addition, DM is also able to influence renin angiotensin system (RAS) increasing angiotensin II (AngII) synthesis which has an important role on LVH development. The RAS main enzyme, responsible for the convertion of angiotensin I (AngI) converting to AngII, is the angiotensin converting enzyme (ACE), target of several population and experimental studies related to its insertion/ deletion (I/D) ACE gene polymorphism. Little is known about the I/D ACE gene polymorphism and DM influence on LVH development, although it has already been demonstrated that animals with increased number of ACE gene copies present increased susceptibility to develop this complication under an additional pathologic stimulus. Thus, the aim of this study is to evaluate the influence of increased ACE gene copies on DCMP development, identifying the correlation between RAS and LVH markers. We suggest that the association between I/D ACE gene polymorphism and DM could trigger RAS and LVH markers alterations, which could be a therapeutic target on DCMP development prevention or control.

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