Autophagy in metabolic syndrome: breaking the wheel by targeting the renin-angiotensin system
ORCID
Latha Ramalingam: 0000-0002-4856-7327
Document Type
Article
Date
2-2020
Keywords
Autophagy, Obesity
Disciplines
Nutrition
Description/Abstract
Metabolic syndrome (MetS) is a complex, emerging epidemic which disrupts the metabolic homeostasis of several organs, including liver, heart, pancreas, and adipose tissue. While studies have been conducted in these research areas, the pathogenesis and mechanisms of MetS remain debatable. Lines of evidence show that physiological systems, such as the renin-angiotensin system (RAS) and autophagy play vital regulatory roles in MetS. RAS is a pivotal system known for controlling blood pressure and fluid balance, whereas autophagy is involved in the degradation and recycling of cellular components, including proteins. Although RAS is activated in MetS, the interrelationship between RAS and autophagy varies in glucose homeostatic organs and their cross talk is poorly understood. Interestingly, autophagy is attenuated in the liver during MetS, whereas autophagic activity is induced in adipose tissue during MetS, indicating tissue-specific discordant roles. We discuss in vivo and in vitro studies conducted in metabolic tissues and dissect their tissue-specific effects. Moreover, our review will focus on the molecular mechanisms by which autophagy orchestrates MetS and the ways future treatments could target RAS in order to achieve metabolic homeostasis.
Recommended Citation
Menikdiwela KR, Ramalingam L, Rasha F, Wang S, Dufour JM, Kalupahana NS, Sunahara KKS, Martins JO, Moustaid-Moussa N. Autophagy in metabolic syndrome: breaking the wheel by targeting the renin-angiotensin system. Cell Death Dis. 2020 Feb 3;11(2):87. doi: 10.1038/s41419-020-2275-9. PMID: 32015340; PMCID: PMC6997396.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
