Evidence map›Paper›PMID 28219767›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2017

The biochemical alterations underlying post-burn hypermetabolism.

Christopher Auger, Osai Samadi, Marc G Jeschke

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
–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

66 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. The effectiveness and potential regulatory mechanism ofFrontiers in cell and developmental biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Pathophysiology of Severe Burn Injuries: New Therapeutic Opportunities From a Systems Perspective.Journal of burn care & research : official publication of the American Burn Association · 2024
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Adipose Tissue Remodeling in Pathophysiology.Annual review of pathology · 2023
    Review
  20. Observational

6 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

3 authors.

Christopher AugerRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario, M4N 3M5, Canada.
Osai SamadiRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario, M4N 3M5, Canada.
Marc G JeschkeRoss Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto, Ontario, M4N 3M5, Canada. Electronic address: marc.jeschke@sunnybrook.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 GM087285
6 · The paper itself

Abstract

A severe burn can trigger a hypermetabolic state which lasts for years following the injury, to the detriment of the patient. The drastic increase in metabolic demands during this phase renders it difficult to meet the body's nutritional requirements, thus increasing muscle, bone and adipose catabolism and predisposing the patient to a host of disorders such as multi-organ dysfunction and sepsis, or even death. Despite advances in burn care over the last 50 years, due to the multifactorial nature of the hypermetabolic phenomenon it is difficult if not impossible to precisely identify and pharmacologically modulate the biological mediators contributing to this substantial metabolic derangement. Here, we discuss biomarkers and molecules which play a role in the induction and mediation of the hypercatabolic condition post-thermal injury. Furthermore, this thorough review covers the development of the factors released after burns, how they induce cellular and metabolic dysfunction, and how these factors can be targeted for therapeutic interventions to restore a more physiological metabolic phenotype after severe thermal injuries. This article is part of a Special Issue entitled: Immune and Metabolic Alterations in Trauma and Sepsis edited by Dr. Raghavan Raju.

Indexed as

AnimalsBurnsHumansMultiple Organ FailureSepsisBurnsCatabolismHypermetabolismInsulin resistanceMitochondriaTrauma

Identifiers

PMID28219767
PMCPMC5563481

What OpenQuestion holds

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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.