Sestrins: A new kid for stroke treatment?

Xudan Shi, Liang Xu, Jay Malagult, Jiping Tang, Min Yan, John H. Zhang

Research output: Contribution to journalReview articlepeer-review

Abstract

Background: The sestrin family includes several conserved stress-induced proteins that contribute to the maintenance of homeostasis, DNA stability and cell viability in response to various types of injuries. Objective: It is well established that the protective functions of AMP-dependent protein kinase (AMPK) and/or mammalian target of rapamycin (mTOR) are regulated by sestrins. Additionally, it has been revealed that sestrins are able to protect cells from oxidative stress by scavenging reactive oxygen species (ROS). Method: The essential involvement of sestrins in mTORC1 inhibition and ROS scavenging signaling pathways, which modulate metabolism homeostasis and regulate autophagy, indicates that sestrins may serve as a potential agent for cell growth, development, metabolism, and neurodegenerative disorders. However, the potential role of sestrins in stroke has not been discussed and summarized. Results & Conclusion: Based on the current understanding of sestrins, it is believed that sestrins are one of the potential endogenous protective molecules/mechanisms following cerebral stroke, which are associated with neuronal protection, neuroinflammation suppression, and blood brain barrier preservation. © 2017 Bentham Science Publishers.
Original languageEnglish
Pages (from-to)797-806
Number of pages10
JournalCurrent Drug Delivery
Volume14
Issue number6
DOIs
StatePublished - Aug 6 2017

ASJC Scopus Subject Areas

  • Pharmaceutical Science

Keywords

  • AMP-dependent protein kinase
  • Mammalian target of rapamycin
  • Reactive oxygen species
  • Redox
  • Sestrins
  • Heat-Shock Proteins/metabolism
  • Reactive Oxygen Species/metabolism
  • Humans
  • Signal Transduction/physiology
  • Animals
  • Stroke/metabolism
  • Nuclear Proteins/metabolism
  • AMP-Activated Protein Kinases/metabolism
  • TOR Serine-Threonine Kinases/metabolism

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