Evidence map›Paper›PMID 19639232›Full record

ArticleInternational journal of molecular medicine2009

Microarray analysis suggests that burn injury results in mitochondrial dysfunction in human skeletal muscle.

A Aria Tzika, Dionyssios Mintzopoulos, Michael Mindrinos, Jiangwen Zhang, Laurence G Rahme, Ronald G Tompkins

Open access · bronzeAbstract read
In one paragraph

Article in International journal of molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021
    Review
  5. Article
  6. Review
  7. The Role of Mitochondrial Stress in Muscle Wasting Following Severe Burn Trauma.Journal of burn care & research : official publication of the American Burn Association · 2018
    Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Uncoupled skeletal muscle mitochondria contribute to hypermetabolism in severely burned adults.American journal of physiology. Endocrinology and metabolism · 2014
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Role of the PPAR-α agonist fenofibrate in severe pediatric burn.Burns : journal of the International Society for Burn Injuries · 2012
    Review
  18. Article
  19. Article
  20. Long-Term Skeletal Muscle Mitochondrial Dysfunction is Associated with Hypermetabolism in Severely Burned Children.Journal of burn care & research : official publication of the American Burn Association
    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.

A Aria TzikaNMR Surgical Laboratory, Department of Surgery, Massachusetts General and Shriners Hospitals, Harvard Medical School, Boston, MA 02114, USA. atzika@hms.harvard.edu
Dionyssios Mintzopoulos
Michael Mindrinos
Jiangwen Zhang
Laurence G Rahme
Ronald G Tompkins
Harvard University · US

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHRISTOPHER P DUGGAN · 1994 to 2026
$31.6M
WOUND HEALINGP50GM021700 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI MARTYN, JEEVENDRA · 1985 to 2017
$27.2M
NIDDK NIH HHS P30 DK040561NIGMS NIH HHS P50 GM021700NIGMS NIH HHS P50GM021700
6 · The paper itself

Abstract

Burn injuries to extensive areas of the body are complicated by muscle catabolism. Elucidating the molecular mechanisms that mediate this catabolism may facilitate the development of a medical intervention. Here, we assessed the functional classification of genes that were differentially expressed in skeletal muscle following burn injury in 19 children (5.2+/-4.0 years of age), (64+/-15% total burn surface area, TBSA) relative to 13 healthy controls (11.9+/-6.0 years of age). Microarray analysis of samples taken within 10 days of burn injury revealed altered expression of a variety of genes, including some involved in cell and organelle organization and biogenesis, stress response, wound response, external stimulus response, regulation of apoptosis and intracellular signaling. The genes that encode peroxisome proliferator-activated receptors (PPARs; 3 isotypes PPARalpha, PPARgamma and PPARdelta also known as PPARbeta or PPARbeta/delta), which may serve as transcriptional nodal points and therapeutic targets for metabolic syndromes, were among those affected. In particular, expression of the main mitochondrial biogenesis factor PPARgamma-1beta (or PGC-1beta) was downregulated (P<0.0001), while the expression of PPARdelta was upregulated (P<0.001). Expression of PGC-1alpha, the closest homolog of PGC-1beta was upregulated (P=0.0037), and expression of the gene encoding mitochodrial uncoupling protein 2 (UCP2) was also upregulated (P=0.008). These results suggest that altered PPAR and mitochondrial gene expression soon after burn injury may lead to metabolic and mitochondrial dysfunction in human skeletal muscle.

Indexed as

Oligonucleotide Array Sequence AnalysisAdolescentBurnsCarrier ProteinsChildChild, PreschoolGene Expression ProfilingGene Expression RegulationHeat-Shock ProteinsHumansInfantIon ChannelsMitochondriaMitochondrial ProteinsMuscle, SkeletalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCarrier ProteinsHeat-Shock ProteinsIon ChannelsMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR alphaPPAR deltaPPARGC1A protein, humanPPARGC1B protein, humanRNA-Binding ProteinsRNA, MessengerTranscription FactorsUCP2 protein, humanUncoupling Protein 2

Identifiers

PMID19639232
PMCPMC3207251
OpenAlexW2058314141

What OpenQuestion holds

Textmetadata
LicenceTDM
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.