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Adipose tissue plasticity mediated by the counterregulatory axis of the renin‐angiotensin system: Role of Mas and MrgD receptors.

Authors :
Proença, Ana Beatriz
Medeiros, Gabriela Rodrigues
Reis, Guilherme dos Santos
Losito, Luiza da França
Ferraz, Luiza Mazzali
Bargut, Thereza Cristina Lonzetti
Soares, Nícia Pedreira
Alexandre‐Santos, Beatriz
Campagnole‐Santos, Maria Jose
Magliano, D'Angelo Carlo
Nobrega, Antonio Claudio Lucas da
Santos, Robson Augusto Souza
Frantz, Eliete Dalla Corte
Source :
Journal of Cellular Physiology; Jun2024, Vol. 239 Issue 6, p1-13, 13p
Publication Year :
2024

Abstract

The renin‐angiotensin system (RAS) is an endocrine system composed of two main axes: the classical and the counterregulatory, very often displaying opposing effects. The classical axis, primarily mediated by angiotensin receptors type 1 (AT1R), is linked to obesity‐associated metabolic effects. On the other hand, the counterregulatory axis appears to exert antiobesity effects through the activation of two receptors, the G protein‐coupled receptor (MasR) and Mas‐related receptor type D (MrgD). The local RAS in adipose organ has prompted extensive research into white adipose tissue and brown adipose tissue (BAT), with a key role in regulating the cellular and metabolic plasticity of these tissues. The MasR activation favors the brown plasticity signature in the adipose organ by improve the thermogenesis, adipogenesis, and lipolysis, decrease the inflammatory state, and overall energy homeostasis. The MrgD metabolic effects are related to the maintenance of BAT functionality, but the signaling remains unexplored. This review provides a summary of RAS counterregulatory actions triggered by Mas and MrgD receptors on adipose tissue plasticity. Focus on the effects related to the morphology and function of adipose tissue, especially from animal studies, will be given targeting new avenues for treatment of obesity‐associated metabolic effects. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00219541
Volume :
239
Issue :
6
Database :
Complementary Index
Journal :
Journal of Cellular Physiology
Publication Type :
Academic Journal
Accession number :
177842007
Full Text :
https://doi.org/10.1002/jcp.31265