title: Autophagy in sepsis: Degradation into exhaustion?
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.
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Jeffery
authors.initials: J
authors.lastname: Ho
authors.affiliation: b State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences and Department of Medicine and Therapeutics , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Jun
authors.initials: J
authors.lastname: Yu
authors.affiliation: b State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences and Department of Medicine and Therapeutics , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Sunny H
authors.initials: SH
authors.lastname: Wong
authors.affiliation: c School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Lin
authors.initials: L
authors.lastname: Zhang
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Liu
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Wai T
authors.initials: WT
authors.lastname: Wong
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Czarina C H
authors.initials: CC
authors.lastname: Leung
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Gordon
authors.initials: G
authors.lastname: Choi
authors.affiliation: d The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Maggie H T
authors.initials: MH
authors.lastname: Wang
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Tony
authors.initials: T
authors.lastname: Gin
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: Matthew T V
authors.initials: MT
authors.lastname: Chan
authors.affiliation: a Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.|b State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences and Department of Medicine and Therapeutics , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
authors.forename: William K K
authors.initials: WK
authors.lastname: Wu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001343:Autophagy / Q000276:immunology / Q000502:physiology*; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D008928:Mitochondria / Q000378:metabolism*; D018805:Sepsis / Q000276:immunology / Q000378:metabolism*
chemical_list: D016207:Cytokines
keywords: apoptosis; autophagy; immunity; mitochondrial function; sepsis