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.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Menikdiwela KR,Ramalingam L,Rasha F,Wang S,Dufour JM,Kalupahana NS,Sunahara KKS,Martins JO,Moustaid-Moussa Ndoi
10.1038/s41419-020-2275-9subject
Has Abstractpub_date
2020-02-03 00:00:00pages
87issue
2issn
2041-4889pii
10.1038/s41419-020-2275-9journal_volume
11pub_type
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