Evidence map›Paper›PMID 27172163›Full record

ReviewAutophagy2016

Autophagy in sepsis: Degradation into exhaustion?

Jeffery Ho, Jun Yu, Sunny H Wong, Lin Zhang, Xiaodong Liu, Wai T Wong, Czarina C H Leung, Gordon Choi, Maggie H T Wang, Tony Gin and 2 more

Abstract readReview
In one paragraph

Review in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

91 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  19. [HTD4010 attenuates myocardial injury in mice with septic cardiomyopathy by promoting autophagyNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  20. Review

31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Jeffery Hoa Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Jun Yub 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.
Sunny H Wongb 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.
Lin Zhangc School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Xiaodong Liua Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Wai T Wonga Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Czarina C H Leunga Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Gordon Choia Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Maggie H T Wangd The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Tony Gina Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
Matthew T V Chana Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.
William K K Wua Department of Anesthesia and Intensive Care , The Chinese University of Hong Kong, Hong Kong Special Administrative Region , China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsApoptosisAutophagyCytokinesHumansImmunity, InnateMitochondriaSepsisCytokinesapoptosisautophagyimmunitymitochondrial functionsepsis

Identifiers

PMID27172163
PMCPMC4990998

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.