Evidence map›Paper›PMID 37397587›Full record

ReviewWorld journal of critical care medicine2023

Sepsis-induced mitochondrial dysfunction: A narrative review.

Wagner Nedel, Caroline Deutschendorf, Luis Valmor Cruz Portela

Abstract readReview
In one paragraph

Review in World journal of critical care medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
–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

57 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. [Thymosin β4 inhibits pyroptosis in BV2 microglial cells: a mechanistic studyZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  10. mRedox biology · 2026
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Observational
  16. Sepsis and the immunometabolic inflammatory response.npj metabolic health and disease · 2026
    Review
  17. Article
  18. Article
  19. Review
  20. 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

3 authors.

Wagner NedelIntensive Care Unit, Grupo Hospitalar Conceição, Porto Alegre 91350200, Brazil.
Caroline DeutschendorfInfection Control Committee, Hospital de Clínicas de Porto Alegre, Porto Alegre 90410-000, Brazil.
Luis Valmor Cruz PortelaLaboratory of Neurotrauma and Biomarkers, Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre 90035-003, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis represents a deranged and exaggerated systemic inflammatory response to infection and is associated with vascular and metabolic abnormalities that trigger systemic organic dysfunction. Mitochondrial function has been shown to be severely impaired during the early phase of critical illness, with a reduction in biogenesis, increased generation of reactive oxygen species and a decrease in adenosine triphosphate synthesis of up to 50%. Mitochondrial dysfunction can be assessed using mitochondrial DNA concentration and respirometry assays, particularly in peripheral mononuclear cells. Isolation of monocytes and lymphocytes seems to be the most promising strategy for measuring mitochondrial activity in clinical settings because of the ease of collection, sample processing, and clinical relevance of the association between metabolic alterations and deficient immune responses in mononuclear cells. Studies have reported alterations in these variables in patients with sepsis compared with healthy controls and non-septic patients. However, few studies have explored the association between mitochondrial dysfunction in immune mononuclear cells and unfavorable clinical outcomes. An improvement in mitochondrial parameters in sepsis could theoretically serve as a biomarker of clinical recovery and response to oxygen and vasopressor therapies as well as reveal unexplored pathophysiological mechanistic targets. These features highlight the need for further studies on mitochondrial metabolism in immune cells as a feasible tool to evaluate patients in intensive care settings. The evaluation of mitochondrial metabolism is a promising tool for the evaluation and management of critically ill patients, especially those with sepsis. In this article, we explore the pathophysiological aspects, main methods of measurement, and the main studies in this field.

Indexed as

InflammationMitochondriaMitochondrial dysfunctionOxidative phosphorylationRespirometrySepsis

Identifiers

PMID37397587
PMCPMC10308342

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Registered trials

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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.