Evidence map›Paper›PMID 39513896›Full record

ReviewCells2024

Mitochondrial Dysfunction and Metabolic Disturbances Induced by Viral Infections.

Sandra E Pérez, Monika Gooz, Eduardo N Maldonado

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Reversible Secondary Carnitine Deficiency Associated With ChronicClinical medicine insights. Case reports · 2026
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. The Essential Role of Mitochondrial Dynamics in Viral Infections.International journal of molecular sciences · 2025
    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

3 authors.

Sandra E PérezCentro de Investigación Veterinaria de Tandil (CIVETAN), UNCPBA-CICPBA-CONICET, Campus Universitario, Tandil CC7000, Buenos Aires, Argentina.
Monika GoozDepartment of Drug Discovery & Biomedical Sciences, Medical University of South Carolina, DD 506 Drug Discovery Building, 70 President Street, MSC 139, Charleston, SC 29425, USA.ORCID 0000-0001-6404-5070
Eduardo N MaldonadoDepartment of Drug Discovery & Biomedical Sciences, Medical University of South Carolina, DD 506 Drug Discovery Building, 70 President Street, MSC 139, Charleston, SC 29425, USA.ORCID 0000-0002-5285-3027

Funding

South Carolina Clinical & Translational Research Institute (SCTR)UL1TR001450 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T., FLUME, PATRICK A · 2015 to 2024
$41.1M
ANPCyT PICT2019-2019-00436Chan Zuckerberg Initiative and the Silicon Valley Community Foundation IS1R-0000000014High-Innovation High Risk-Award High-Innovation High Risk-AwardSouth Carolina Translational Research: Pilot Project UL1 TR001450-SCTR
6 · The paper itself

Abstract

Viruses are intracellular parasites that utilize organelles, signaling pathways, and the bioenergetics machinery of the cell to replicate the genome and synthesize proteins to build up new viral particles. Mitochondria are key to supporting the virus life cycle by sustaining energy production, metabolism, and synthesis of macromolecules. Mitochondria also contribute to the antiviral innate immune response. Here, we describe the different mechanisms involved in virus-mitochondria interactions. We analyze the effects of viral infections on the metabolism of glucose in the Warburg phenotype, glutamine, and fatty acids. We also describe how viruses directly regulate mitochondrial function through modulation of the activity of the electron transport chain, the generation of reactive oxygen species, the balance between fission and fusion, and the regulation of voltage-dependent anion channels. In addition, we discuss the evasion strategies used to avoid mitochondrial-associated mechanisms that inhibit viral replication. Overall, this review aims to provide a comprehensive view of how viruses modulate mitochondrial function to maintain their replicative capabilities.

Indexed as

Metabolic DiseasesMitochondriaMitochondrial DiseasesVirus DiseasesHumansMitochondrial DynamicsReactive Oxygen SpeciesVoltage-Dependent Anion ChannelsReactive Oxygen SpeciesVoltage-Dependent Anion Channelselectron transport chainfatty acidsglucoseglutamineinnate immunitymetabolic reprogrammingmitochondriareactive oxygen speciesVDACsvirusWarburg

Identifiers

PMID39513896
PMCPMC11545457

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.