Evidence map›Paper›PMID 27382037›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2016

Hypermetabolism and hypercatabolism of skeletal muscle accompany mitochondrial stress following severe burn trauma.

John O Ogunbileje, Craig Porter, David N Herndon, Tony Chao, Doaa R Abdelrahman, Anastasia Papadimitriou, Maria Chondronikola, Teresa A Zimmers, Paul T Reidy, Blake B Rasmussen and 1 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

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  12. Burns & trauma · 2024
    Article
  13. Article
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  16. Observational
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  20. [Roles of adenosine monophosphate activated protein kinase in skeletal muscle atrophy in rats with severe scald].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021
    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

11 authors at 4 institutions in 1 country.

John O OgunbilejeMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Surgery, University of Texas Medical Branch, Galveston, Texas; joogunbi@utmb.edu.
Craig PorterMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Surgery, University of Texas Medical Branch, Galveston, Texas;
David N HerndonMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Surgery, University of Texas Medical Branch, Galveston, Texas;
Tony ChaoMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Surgery, University of Texas Medical Branch, Galveston, Texas;
Doaa R AbdelrahmanMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Surgery, University of Texas Medical Branch, Galveston, Texas;
Anastasia PapadimitriouMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Nutrition and Metabolism, University of Texas Medical Branch, Galveston, Texas;
Maria ChondronikolaMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas;
Teresa A ZimmersDepartment of Surgery, Indiana University School of Medicine, Indianapolis, Indiana;
Paul T ReidyDepartment of Nutrition and Metabolism, University of Texas Medical Branch, Galveston, Texas;
Blake B RasmussenDepartment of Nutrition and Metabolism, University of Texas Medical Branch, Galveston, Texas;
Labros S SidossisMetabolism Unit, Shriners Hospitals for Children, Galveston, Texas; Department of Surgery, University of Texas Medical Branch, Galveston, Texas; Department of Kinesiology and Health, Rutgers University, New Brunswick, New Jersey; and Robert Wood Johnson Medical School, Rutgers University, New Brunswick, New Jersey.
Shriners Hospitals for Children - Galveston · USThe University of Texas Medical Branch at Galveston · USIndiana University School of MedicineJohnson University · US

Funding

Project 9: The role of androgen/corticosteroid in fat, muscle and glucose metabolism of burn victimsP50GM060338 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HERNDON, DAVID N. · 2000 to 2017
$24.2M
UTMB Clinical and Translational Science AwardUL1TR000071 · NCATS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BRASIER, ALLAN R. · 2012 to 2014
$14.4M
MODULATION OF THE POSTBURN HYPERMETABOLIC RESPONSER01GM056687 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HERNDON, DAVID N. · 1998 to 2017
$9.0M
POSTDOCTORAL TRAINING IN TRAUMA &BURNST32GM008256 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Celeste Campbell Finnerty, Oscar E. Suman-Vejas · 1990 to 2026
$4.0M
Nutritional and Contractile Regulation of Muscle GrowthR01AR049877 · NIAMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI RASMUSSEN, BLAKE B · 2004 to 2012
$3.3M
Myostatin Family Signaling in Burn-Injury Related Muscle WastingR01GM092758 · NIGMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ZIMMERS, TERESA A · 2010 to 2014
$1.6M
NCATS NIH HHS UL1 TR000071NIAMS NIH HHS R01 AR049877NIGMS NIH HHS P50 GM060338NIGMS NIH HHS R01 GM056687NIGMS NIH HHS R01 GM092758NIGMS NIH HHS T32 GM008256
6 · The paper itself

Abstract

Burn trauma results in prolonged hypermetabolism and skeletal muscle wasting. How hypermetabolism contributes to muscle wasting in burn patients remains unknown. We hypothesized that oxidative stress, cytosolic protein degradation, and mitochondrial stress as a result of hypermetabolism contribute to muscle cachexia postburn. Patients (n = 14) with burns covering >30% of their total body surface area were studied. Controls (n = 13) were young healthy adults. We found that burn patients were profoundly hypermetabolic at both the skeletal muscle and systemic levels, indicating increased oxygen consumption by mitochondria. In skeletal muscle of burn patients, concurrent activation of mTORC1 signaling and elevation in the fractional synthetic rate paralleled increased levels of proteasomes and elevated fractional breakdown rate. Burn patients had greater levels of oxidative stress markers as well as higher expression of mtUPR-related genes and proteins, suggesting that burns increased mitochondrial stress and protein damage. Indeed, upregulation of cytoprotective genes suggests hypermetabolism-induced oxidative stress postburn. In parallel to mtUPR activation postburn, mitochondrial-specific proteases (LONP1 and CLPP) and mitochondrial translocases (TIM23, TIM17B, and TOM40) were upregulated, suggesting increased mitochondrial protein degradation and transport of preprotein, respectively. Our data demonstrate that proteolysis occurs in both the cytosolic and mitochondrial compartments of skeletal muscle in severely burned patients. Increased mitochondrial protein turnover may be associated with increased protein damage due to hypermetabolism-induced oxidative stress and activation of mtUPR. Our results suggest a novel role for the mitochondria in burn-induced cachexia.

Indexed as

Oxidative StressOxygen ConsumptionAdolescentAdultATP-Dependent ProteasesBlotting, WesternBody Surface AreaBurnsCachexiaCase-Control StudiesEndopeptidase ClpFemaleHumansMaleMechanistic Target of Rapamycin Complex 1MetabolismATP-Dependent ProteasesClpP protein, humanEndopeptidase ClpLONP1 protein, humanMechanistic Target of Rapamycin Complex 1Mitochondrial Membrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsMitochondrial ProteinsMultiprotein ComplexesMuscle ProteinsProteasome Endopeptidase ComplexRNA, MessengerTIMM17B protein, humanTIMM23 protein, humanTOMM40 protein, humanTOR Serine-Threonine Kinasesburn injurycachexiahypermetabolism-induced oxidative stressmitochondrial unfolded protein responsemitochondria proteases

Identifiers

PMID27382037
PMCPMC5005969
OpenAlexW2469703900

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.