Evidence map›Paper›PMID 31494084›Full record

ReviewChest2020

Mitochondria and Critical Illness.

Gerald S Supinski, Elizabeth A Schroder, Leigh Ann Callahan

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Chest, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07018843 (Metabolic Characterisation of Critically Ill Patients), which is not on this map. Cited by 123 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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.

NCT07018843 not yet recruitingnot on this mapstarted 2025, after this paper: background citation

Metabolic Characterisation of Critically Ill Patients: An Observational Study Focusing on Mitochondria

TypeobservationalSponsorUniversity Hospital Southampton NHS Foundation TrustRan2025 to 2026Enrolled20ConditionsCritical Illness
3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Observational
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  10. Review
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  18. Review
  19. Article
  20. Acute lung injury: pathogenesis and treatment.Journal of translational medicine · 2025
    Review

63 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Gerald S SupinskiDivision of Pulmonary, Critical Care and Sleep Medicine, University of Kentucky, Lexington, KY.
Elizabeth A SchroderDivision of Pulmonary, Critical Care and Sleep Medicine, University of Kentucky, Lexington, KY.
Leigh Ann CallahanDivision of Pulmonary, Critical Care and Sleep Medicine, University of Kentucky, Lexington, KY. Electronic address: lacall2@email.uky.edu.
University of Kentucky · US

Funding

Treatment of Skeletal Muscle Dysfunction in ICU PatientsR01HL113494 · NHLBI · UNIVERSITY OF KENTUCKY · PI SUPINSKI, GERALD S. · 2013 to 2016
$2.3M
Mitochondrially Targeted Therapies for Sepsis Induced Diaphragm DysfunctionR01HL141356 · NHLBI · UNIVERSITY OF KENTUCKY · PI CALLAHAN, LEIGH A, SCHRODER STUMPF, ELIZABETH A · 2018 to 2021
$2.2M
Effects of Sleep Deprivation on Infection Induced Organ FailureR01HL112085 · NHLBI · UNIVERSITY OF KENTUCKY · PI CALLAHAN, LEIGH A · 2013 to 2016
$1.5M
Respiratory Muscle WeaknessI01BX002132 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI SUPINSKI, GERALD S. · 2015 to 2018
–
BLRD VA I01 BX002132NHLBI NIH HHS R01 HL112085NHLBI NIH HHS R01 HL113494NHLBI NIH HHS R01 HL141356
6 · The paper itself

Abstract

Classically, mitochondria have largely been believed to influence the development of illness by modulating cell metabolism and determining the rate of production of high-energy phosphate compounds (eg, adenosine triphosphate). It is now recognized that this view is simplistic and that mitochondria play key roles in many other processes, including cell signaling, regulating gene expression, modulating cellular calcium levels, and influencing the activation of cell death pathways (eg, caspase activation). Moreover, these multiple mitochondrial functional characteristics are now known to influence the evolution of cellular and organ function in many disease states, including sepsis, ICU-acquired skeletal muscle dysfunction, acute lung injury, acute renal failure, and critical illness-related immune function dysregulation. In addition, diseased mitochondria generate toxic compounds, most notably released mitochondrial DNA, which can act as danger-associated molecular patterns to induce systemic toxicity and damage multiple organs throughout the body. This article reviews these evolving concepts relating mitochondrial function and acute illness. The discussion is organized into four sections: (1) basics of mitochondrial physiology; (2) cellular mechanisms of mitochondrial pathophysiology; (3) critical care disease processes whose initiation and evolution are shaped by mitochondrial pathophysiology; and (4) emerging treatments for mitochondrial dysfunction in critical illness.

Indexed as

Acute Lung InjuryAlarminsAntioxidantsCesiumCritical IllnessDNA, MitochondrialHumansMelatoninMitochondriaMuscle, SkeletalMuscular DiseasesOrganelle BiogenesisResveratrolSepsisAlarminsAntioxidantsCesiumDNA, MitochondrialMelatoninResveratrolcritical illnesslung injurymitochondriamuscle dysfunctionsepsis

Identifiers

PMID31494084
PMCPMC7005375
OpenAlexW2971657164

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.