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Characterizing NADPH oxidase-dependent ROS production and redox signalling in hiPSC from normotensive and hypertensive subjects

Grant number: 17/26460-9
Support Opportunities:Scholarships abroad - Research Internship - Master's degree
Effective date (Start): March 31, 2018
Effective date (End): September 20, 2018
Field of knowledge:Biological Sciences - Biochemistry - Metabolism and Bioenergetics
Principal Investigator:Lygia da Veiga Pereira
Grantee:Raquel Delgado Sarafian
Supervisor: Rhian Merry Touyz
Host Institution: Instituto de Biociências (IB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: University of Glasgow, Scotland  
Associated to the scholarship:16/20650-8 - Assessment of hIPSC- derived hepatocytes as a model to study the responsiveness losartan in vitro, BP.MS


Hypertension is an important risk factor for various cardiovascular diseases, such as stroke, acute myocardial infarction and chronic kidney disease. It is a complex, multifactorial disease whose cellular mechanisms are not well understood. Recently several studies have focused on the role of oxidative stress regarding to the development of hypertension. Increasing evidence over the last decades indicates an association between reactive oxygen species (ROS) and arterial hypertension. ROS are essential for cellular physiology, but in an unbalanced situation an exacerbated production of ROS can damage cellular components and trigger pathological processes. Among the different ROS sources that are present in the heart, NADPH oxidases (Noxs) are particularly important because they are involved into many features of heart dysfunction. However, in human, even if redox regulation of some of signaling proteins is well established, the role of Noxs in cardiac pathologies caused by hypertension and the relation to Nox-derived ROS and hypertension are misunderstood. The elucidation of mechanisms involved in NOX-dependent regulation of cardiac remodeling may lead to new therapeutic targets for heart failure associated with hypertension. In this scenario, human induced pluripotent stem cells (hiPSC), which are already recognized as a tool for modeling various diseases in vitro, can be a powerful tool for understanding cellular mechanisms in response to oxidative stress in hypertension - induced cardiomyocyte dysfunction. Thus, in the present project, we propose to use hiPSC-derived cardiomyocytes from normotensive, responsive and resistant hypertensive patients as a source for the study of Nox.

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