Evidence map›Paper›PMID 27443317›Full record

ArticleJournal of intensive care medicine2017

Measurement of Mitochondrial Respiration and Motility in Acute Care: Sepsis, Trauma, and Poisoning.

David H Jang, John C Greenwood, Meghan B Spyres, David M Eckmann

Abstract read
In one paragraph

Article in Journal of intensive care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

  1. Targeting Mitochondrial Dysfunction in Acute Organophosphate Toxicity: A Preliminary Evaluation of Cyclosporine A.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2026
    Article
  2. Article
  3. Article
  4. Association Between Myocardial Dysfunction and Septic Shock.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Blood Cells as a Cellular Biomarker for Mitochondrial Function in a Experimental Model of Acute Carbon Monoxide Poisoning with Treatment.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Investigation of Cerebral Mitochondrial Injury in a Porcine Survivor Model of Carbon Monoxide Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2024
    Article
  14. Assessing Platelet Mitochondrial Dysfunction in a Murine Model of Acute Acetaminophen Toxicity.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023
    Article
  15. Sepsis-induced mitochondrial dysfunction: A narrative review.World journal of critical care medicine · 2023
    Review
  16. Alteration in Cerebral Metabolism in a Rodent Model of Acute Sub-lethal Cyanide Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2023
    Article
  17. Article
  18. Elevated LDL-C, high blood pressure, and low peakFrontiers in molecular biosciences · 2023
    Article
  19. Article
  20. Emerging cellular-based therapies in carbon monoxide poisoning.American journal of physiology. Cell physiology · 2021
    Review
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

4 authors.

David H JangDepartment of Emergency Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA david.jang@uphs.upenn.edu.
John C GreenwoodDepartment of Emergency Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Meghan B SpyresDepartment of Emergency Medicine, Section of Medical Toxicology, University of Southern California, Los Angeles, CA, USA.
David M EckmannDepartment of Anesthesiology and Critical Care, University of Pennsylvania, Philadelphia, PA, USA.

Funding

Enabling Medical Research Growth in Emergency MedicineK12HL109009 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KIMMEL, STEPHEN E. · 2011 to 2015
$3.4M
NHLBI NIH HHS K12 HL109009
6 · The paper itself

Abstract

Metabolic biomarkers have potentially wider use in disease diagnosis and prognosis as well as in monitoring disease response to treatment. While biomarkers such as interleukins, microRNA, and lactate have been proposed for disease surveillance, there are still conflicting results regarding their clinical utility. Treatment of commonly encountered disease of acute care such as sepsis, trauma, and poisoning often relies on clinical diagnosis and therapy guided by use of surrogate markers of illness severity. The measurement of mitochondrial function, including respiration and motility, may offer superior alternatives to such markers. Assessing mitochondrial function in a clinical context has the potential to impact the area of acute care in terms of diagnosis, prognosis, and treatment. The study of mitochondrial bioenergetics has become critical in understanding the pathophysiology and treatment of complex diseases such as diabetes and cardiovascular disorders.

Indexed as

Cell RespirationCritical CareBiomarkersCritical IllnessHumansMitochondriaMonitoring, PhysiologicPoisoningReactive Oxygen SpeciesSepsisWounds and InjuriesBiomarkersReactive Oxygen Speciesbioenergeticsmedical toxicologymitochondriamitochondrial motilityresuscitationsepsis

Identifiers

PMID27443317
PMCPMC6902634

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.