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

Grant number: 23/00966-4
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): May 29, 2023
Effective date (End): May 24, 2024
Field of knowledge:Biological Sciences - Genetics - Human and Medical Genetics
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: McGill University, Montreal, Canada  
Associated to the scholarship:20/03108-0 - Establishment of the in vitro cardiovascular model derived from human Pluripotent Stem Cells (hiPSCs) for functional analysis of Hypertension, BP.DR

Abstract

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 still poorly understood. Recently, several studies have focused on the role of oxidative stress in 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 cardiovascular system, NADPH oxidases (Noxs) are particularly important because they are involved into many features of heart and vascular dysfunction. Particularly in human hypertension, redox signaling regulation and the role of Noxs in cardiovascular pathologies await clarification. The elucidation of mechanisms involved in NOX-dependent regulation of cardiac and vascular remodelling may lead to new therapeutic targets for hypertension and associated diseases. In this scenario, human-induced pluripotent stem cells (hiPSC), which are already recognized as a model for studying various diseases in vitro, can be a powerful tool for understanding cellular mechanisms in response to oxidative stress in hypertension-induced cardiovascular dysfunction. Thus, in the present project, we propose to use hiPSC-derived cardiomyocytes, endothelial cells and vascular smooth muscle cells from normotensive and hypertensive patients to dissect the redox mechanisms whereby Nox regulates cardiovascular function. (AU)

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