Evidence map›Paper›PMID 31713718›Full record

ReviewCurrent nutrition reports2019

Mitochondrial Dysfunction in Critical Illness: Implications for Nutritional Therapy.

Stephen A McClave, Paul E Wischmeyer, Keith R Miller, Arthur R H van Zanten

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current nutrition reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Review
  3. Observational
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. High-resolution plasma metabolomics and thiamine status in critically Ill adult patients.Metabolomics : Official journal of the Metabolomic Society · 2024
    Article
  11. Review
  12. Critical care: A concept analysis.International journal of nursing sciences · 2023
    Review
  13. Sepsis-induced mitochondrial dysfunction: A narrative review.World journal of critical care medicine · 2023
    Review
  14. Article
  15. Article
  16. Observational
  17. 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 at 3 institutions in 2 countries.

Stephen A McClaveDepartment of Medicine, University of Louisville School of Medicine, Louisville, KY, USA. samcclave@louisville.edu.
Paul E WischmeyerDepartment of Anesthesiology, Duke University, Durham, NC, USA.
Keith R MillerDepartment of Surgery, University of Louisville School of Medicine, Louisville, KY, USA.
Arthur R H van ZantenDepartment of Intensive Care Medicine, Gelderse Vallei Hospital, Ede, The Netherlands.
University of Louisville · USDuke University · USZiekenhuis Gelderse Vallei · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of the reviewThis paper will review the evidence for mitochondrial dysfunction in critical illness, describe the mechanisms which lead to multiple organ failure, and detail the implications of this pathophysiologic process on nutritional therapy. RECENT

findingsMitochondria are particularly sensitive to increased oxidative stress in critical illness. The functional and structural abnormalities which occur in this organelle contribute further to the excessive production of reactive oxygen species and the reduction in generation of adenosine triphosphate (ATP). To reduce metabolic demand, mitochondrial dysfunction develops (a process likened to hibernation), which helps sustain the life of the cell at a cost of organ system failure. Aggressive feeding in the early phases of critical illness might inappropriately increase demand at a time when ATP production is limited, further jeopardizing cell survival and potentiating the processes leading to multiple organ failure. Several potential therapies exist which would promote mitochondrial function in the intensive care setting through support of autophagy, antioxidant defense systems, and the biogenesis and recovery of the organelle itself. Nutritional therapy should supplement micronutrients required in the mitochondrial metabolic pathways and provide reduced delivery of macronutrients through slower advancement of feeding in the early phases of critical illness. A better understanding of mitochondrial dysfunction in the critically ill patient should lead to more innovative therapies in the future.

Indexed as

Adenosine TriphosphateAntioxidantsAutophagyCritical CareCritical IllnessEnergy MetabolismHumansMitochondriaMitochondrial DiseasesMultiple Organ FailureNutritional SupportNutrition TherapyOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateAntioxidantsReactive Oxygen SpeciesCritical illnessMitochondrial failureMultiple organ failureNutritional therapy

Identifiers

PMID31713718
OpenAlexW2987626543

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.