Autophagy in sepsis : Degradation into exhaustion?

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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Author(s)

  • Jeffery Ho
  • Jun Yu
  • Sunny H. Wong
  • Lin Zhang
  • Xiaodong Liu
  • And 7 others
  • Wai T. Wong
  • Czarina C. H. Leung
  • Gordon Choi
  • Maggie H. T. Wang
  • Tony Gin
  • Matthew T. V. Chan
  • William K. K. Wu

Detail(s)

Original languageEnglish
Pages (from-to)1073-1082
Number of pages10
Journal / PublicationAutophagy
Volume12
Issue number7
Online published9 Jun 2016
Publication statusPublished - 2016
Externally publishedYes

Abstract

Autophagy is one of the innate immune defense mechanisms against microbial challenges. Previous in vitro and in vivo models of sepsis demonstrated that autophagy was activated initially in sepsis, followed by a subsequent phase of impairment. Autophagy modulation appears to be protective against multiple organ injuries in these murine sepsis models. This is achieved in part by preventing apoptosis, maintaining a balance between the productions of pro- and anti-inflammatory cytokines, and preserving mitochondrial functions. This article aims to discuss the role of autophagy in sepsis and the therapeutic potential of autophagy enhancers.

Research Area(s)

  • apoptosis, autophagy, immunity, mitochondrial function, sepsis, ENDOPLASMIC-RETICULUM STRESS, CONTRACTILE DYSFUNCTION, IMPROVES SURVIVAL, NITRIC-OXIDE, SEPTIC MICE, LUNG INJURY, MITOCHONDRIAL BIOGENESIS, CARDIAC CONTRACTILE, SIGNALING PATHWAY, PROTECTS MICE

Citation Format(s)

Autophagy in sepsis : Degradation into exhaustion? / Ho, Jeffery; Yu, Jun; Wong, Sunny H.; Zhang, Lin; Liu, Xiaodong; Wong, Wai T.; Leung, Czarina C. H.; Choi, Gordon; Wang, Maggie H. T.; Gin, Tony; Chan, Matthew T. V.; Wu, William K. K.

In: Autophagy, Vol. 12, No. 7, 2016, p. 1073-1082.

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review