Evidence map›Paper›PMID 32574708›Full record

ReviewMitochondrion2020

Mitochondria and microbiota dysfunction in COVID-19 pathogenesis.

Jumana Saleh, Carole Peyssonnaux, Keshav K Singh, Marvin Edeas

Open access · bronzeAbstract readReview
In one paragraph

Review in Mitochondrion, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 4 pooled it
6.4field-weighted citation impact, top 3% 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

209 citing papers in PubMed, 4 syntheses or guidelines pooled it, 310 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Impact of Cardiovascular Diseases on COVID-19: A Systematic Review.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Pooled it
  4. Pooled it
  5. Combined Metabolic Activators Accelerates Recovery in Mild-to-Moderate COVID-19.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Trial
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Impact of nutrition on long COVID.Sports medicine and health science · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

149 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

4 authors at 4 institutions in 3 countries.

Jumana SalehCollege of Medicine, Sultan Qaboos University, Oman.
Carole PeyssonnauxUniversité de Paris, INSERM U1016, Institut Cochin, CNRS UMR8104, Faculté de médecine Cochin-Port Royal, Paris, France; Laboratory of Excellence GR-Ex, Paris, France.
Keshav K SinghIntegrated Center for Aging Research, Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Marvin EdeasUniversité de Paris, INSERM U1016, Institut Cochin, CNRS UMR8104, Faculté de médecine Cochin-Port Royal, Paris, France; Laboratory of Excellence GR-Ex, Paris, France. Electronic address: marvin.edeas@inserm.fr.
Institut Cochin · FRInstitut des Maladies Génétiques Imagine · FRSultan Qaboos University · OMUniversity of Alabama at Birmingham · US

Funding

Mitochondria in Prostate Cancer DiversityR01CA204430 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SINGH, KESHAV K · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA204430
6 · The paper itself

Abstract

The COVID-19 pandemic caused by the coronavirus (SARS-CoV-2) has taken the world by surprise into a major crisis of overwhelming morbidity and mortality. This highly infectious disease is associated with respiratory failure unusual in other coronavirus infections. Mounting evidence link the accelerated progression of the disease in COVID-19 patients to the hyper-inflammatory state termed as the "cytokine storm" involving major systemic perturbations. These include iron dysregulation manifested as hyperferritinemia associated with disease severity. Iron dysregulation induces reactive oxygen species (ROS) production and promotes oxidative stress. The mitochondria are the hub of cellular oxidative homeostasis. In addition, the mitochondria may circulate "cell-free" in non-nucleated platelets, in extracellular vesicles and mitochondrial DNA is found in the extracellular space. The heightened inflammatory/oxidative state may lead to mitochondrial dysfunction leading to platelet damage and apoptosis. The interaction of dysfunctional platelets with coagulation cascades aggravates clotting events and thrombus formation. Furthermore, mitochondrial oxidative stress may contribute to microbiota dysbiosis, altering coagulation pathways and fueling the inflammatory/oxidative response leading to the vicious cycle of events. Here, we discuss various cellular and systemic incidents caused by SARS-CoV-2 that may critically impact intra and extracellular mitochondrial function, and contribute to the progression and severity of the disease. It is crucial to understand how these key modulators impact COVID-19 pathogenesis in the quest to identify novel therapeutic targets that may reduce fatal outcomes of the disease.

Indexed as

BetacoronavirusBlood Coagulation DisordersBlood PlateletsCardiolipinsCoronavirus InfectionsCOVID-19DysbiosisHomeostasisHumansInflammationIronMitochondriaMitochondrial DiseasesOxidative StressPandemicsPneumonia, ViralCardiolipinsIronExtracellular mitochondriaHypercoagulabilityHyper-inflammationIronMicrobiotaOxidative stressPlatelet mitochondria

Identifiers

PMID32574708
PMCPMC7837003
OpenAlexW3036360747

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.