EVALUATION OF TREATMENT WITH LIRAGLUTIDE AND SGLT2 INHIBITORS IN INFLAMMATION MEDIATED BY THE ACTION OF microRNAS 21, 145 AND 34A ON The HIF1-ALPHA FACTOR IN PROXIMAL CELLS (HK-2) SUBMITTED TO OXYGEN DEPRIVATION.

• Grant number: 22/08798-0
• Support Opportunities: Scholarships in Brazil - Master
• Start date: May 01, 2023
• End date: May 31, 2024
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Marcelo Costa Batista
• Grantee: Julia Cristine Oliveira
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
• Associated research grant: 19/25493-6 - Obesity: pathophysiology and related therapeutic strategies, AP.TEM

Abstract

Visceral obesity, the nucleus of Metabolic Syndrome (MetS), is conceived as a pathophysiological basis, with an epidemic incidence of cardiovascular events. It has been suggested that MS is a programmable disease, characterized by epigenetic changes in vital genes when exposed to stress in various ways, such as hypoxia associated with inflammation. Epigenetic changes participate in CKD susceptibility and have been investigated as the environment interacts with the renal cell epigenome to contribute to kidney damage. Changes in the expression of miRNAs can cause changes in the pattern of genes that control a series of biological processes, such as: inflammation, lipid metabolism, insulin resistance and adipogenesis. The use of GLP-1 agonists (peptide similar to glucagon 1) and, more recently, inhibitors of renal tubular glucose transport (iSGLT 2) have been related to the higher prevalence of renal function in patients with renal deseases. Considering the importance of cellular adaptive processes in the pathophysiology of tubular kidney injury induced by obesity the aim of this study is evaluate the effect of treatment with GLP1 agonist in association withsGLT2 inhibitor on the modulation of microRNAs 21, 145 and 34a on the expression of inflammatorymediators in proximal cells (HK-2) under oxygen deprivation and stimulated with leptin.