Characterization of the role of Galectin-3 in cardiovascular changes associated with arterial hypertension induced by a high sodium diet.

• Grant number: 24/02931-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: May 01, 2024
• End date: April 30, 2025
• Field of knowledge: Biological Sciences - Pharmacology - Cardiorenal Pharmacology
• Principal Investigator: Rita de Cassia Aleixo Tostes Passaglia
• Grantee: Letícia Yumi Okada
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Arterial hypertension is a pathophysiological condition that affects a large part of the world's population and is one of the main causes of early mortality. It is characterized by persistent elevation in blood pressure, which may be related to genetic and environmental factors, such as excessive consumption of sodium chloride (NaCl). Excess NaCl induces water retention, increased peripheral vascular resistance, changes in the function of the vascular endothelium and in autonomic neural modulation, leading to increased blood volume and blood pressure. Blood vessels are made up of three layers: the intima, the media and the adventitia. Vascular dysfunction associated with arterial hypertension is caused by functional and structural changes in these tunics, and is characterized by changes in reactivity to contractile and vasodilatory agents, increased proliferation and migration of vascular smooth muscle cells (VSMCs) and dysfunction of endothelial cells. These vascular abnormalities are generally associated with the presence of oxidative stress and an inflammatory process. Galectin-3 (Gal-3) is a B-galactoside binding protein that has anti-apoptotic, proliferative and pro-inflammatory properties, regulating several cellular processes, such as cell growth, fibrosis, tissue repair and angiogenesis. It is known that Gal-3 is expressed by VSMCs and is involved in cardiovascular dysfunction and cardiac remodeling in heart failure (HF), mediating inflammatory and cell migration processes. Considering that Gal-3 is used as a biomarker in heart failure (HF) and atherosclerosis, that Gal-3 contributes to the remodeling of the vascular extracellular matrix (ECM), but that its role in arterial hypertension is not yet known, our study will evaluate whether Gal-3 contributes to the vascular dysfunction observed in arterial hypertension. Our hypothesis is that there is an increase in Galectin-3 levels in hypertensive conditions and that this increase is related to cardiovascular dysfunction, initially represented by changes in vascular reactivity and the presence of cardiac and vascular structural changes.