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Role of the senescence in obesity-induced cardiac hypertrophy and the influence of the microRNAs

Grant number: 23/02585-8
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): July 01, 2023
Effective date (End): June 30, 2024
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Gabriela Placoná Diniz
Grantee:Tábatha de Oliveira Silva
Supervisor: Dazhi Wang
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: University of South Florida (USF), United States  
Associated to the scholarship:20/14289-6 - Impact of cellular senescence in Obesity-induced cardiovascular and metabolic dysfunctions in female mice, BP.DR


Obesity is a risk factor related to metabolic and cardiovascular diseases. Recent studies have demonstrated that obesity accelerates aging-related processes, such as cellular senescence. Although senescent cells play important physiological functions, they have a high active metabolism and a senescence-associated secretory profile (SASP) that influence the tissue microenvironment and the function of other tissues. Recent studies have shown that obese male mice have an increase of the white adipose tissue senescence, and the clearance of senescent cells attenuates metabolic disorders associated with obesity. In addition, senescent cells removal attenuates diastolic dysfunction in db/db obese male mice. MicroRNAs (miRNAs) are small non-coding RNAs that reduce mRNAs stability and/or translation, influencing diverse physiological and pathological processes, such as obesity-related cardiometabolic disorders. However, whether cellular senescence plays a role in obesity-induced cardiac hypertrophy in female mice, and whether this event may be influenced by alterations in the cardiac microRNA expression profile remain unknown. In this sense, this study aims to investigate the microRNA expression profile in obesity-induced cardiac hypertrophy in female mice, and the role of cellular senescence in these events. (AU)

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