Evidence map›Paper›PMID 32810382›Full record

ArticleJournal of cellular and molecular medicine2020

Activation of ER stress signalling increases mortality after a major trauma.

Abdikarim Abdullahi, Dalia Barayan, Roohi Vinaik, Li Diao, Nancy Yu, Marc G Jeschke

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 30% of its field
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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. β-Adrenergic blockade attenuates adverse adipose tissue responses after burn.Journal of molecular medicine (Berlin, Germany) · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Interleukin-6 blockade, a potential adjunct therapy for post-burn hypermetabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  11. Review
  12. Article
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

6 authors at 1 institution in 1 country.

Abdikarim AbdullahiFaculty of Medicine, University of Toronto, Toronto, ON, Canada.
Dalia BarayanFaculty of Medicine, University of Toronto, Toronto, ON, Canada.
Roohi VinaikFaculty of Medicine, University of Toronto, Toronto, ON, Canada.
Li DiaoBiological Sciences, Sunnybrook Research Institute, Toronto, ON, Canada.
Nancy YuBiological Sciences, Sunnybrook Research Institute, Toronto, ON, Canada.
Marc G JeschkeFaculty of Medicine, University of Toronto, Toronto, ON, Canada.ORCID 0000-0003-0870-1664
Sunnybrook Health Science Centre · CA

Funding

Hepatic ER stress contributes to morbidity and mortality after burn injury.R01GM087285 · NIGMS · SUNNYBROOK & WOMEN'S COLL HLTH SCIS CTR · PI BOEHNING, DARREN F, JESCHKE, MARC GERHARD · 2010 to 2018
$1.9M
NIGMS NIH HHS R01 GM087285NIH HHS R01-GM087285-01
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) adapts to stress by activating a signalling cascade known as the ER stress response. While ER stress signalling is a central component of the cellular defence against environmental insult, persistent activation is thought to contribute to the progression of various metabolic complications via loss of protein function and cell death. Despite its importance however, whether and how ER stress impacts morbidity and mortality in conditions of hypermetabolism remain unclear. In this study, we discovered that chronic ER stress response plays a role in mediating adverse outcomes that occur after major trauma. Using a murine model of thermal injury, we show that induction of ER stress with Tunicamycin not only increased mortality but also resulted in hepatic damage and hepatic steatosis. Importantly, post-burn treatment with chaperone ER stress inhibitors attenuated hepatic ER stress and improved organ function following injury. Our study identifies ER stress as a potential hub of the signalling network affecting multiple aspects of metabolism after major trauma and as a novel potential molecular target to improve the clinical outcomes of severely burned patients.

Indexed as

AnimalsEndoplasmic ReticulumEndoplasmic Reticulum StressFatty LiverHumansLiverLiver DiseasesMiceSignal TransductionWounds and InjuriesburnsER stresshypermetabolismlivertraumaunfolded protein response

Identifiers

PMID32810382
PMCPMC7520325
OpenAlexW3081077685

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.