Evidence map›Paper›PMID 38927073›Full record

ReviewBiomolecules2024

Mitochondrial Reactive Oxygen Species in Infection and Immunity.

Arunima Mukherjee, Krishna Kanta Ghosh, Sabyasachi Chakrabortty, Balázs Gulyás, Parasuraman Padmanabhan, Writoban Basu Ball

Abstract readReview
In one paragraph

Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed.

  1. Review
  2. Molecular remodelling ofJournal of medical microbiology · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. mRedox biology · 2026
    Review
  10. Article
  11. Review
  12. Article
  13. Selenium and Selenoproteins in Neutrophil Functions.Biological trace element research · 2026
    Review
  14. Review
  15. Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026
    Review
  16. 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

6 authors.

Arunima MukherjeeDepartment of Biological Sciences, School of Engineering and Sciences, SRM University AP Andhra Pradesh, Guntur 522502, Andhra Pradesh, India.ORCID 0000-0002-9597-1867
Krishna Kanta GhoshLee Kong Chian School of Medicine, Nanyang Technological University Singapore, 59 Nanyang Drive, Singapore 636921, Singapore.
Sabyasachi ChakraborttyDepartment of Chemistry, School of Engineering and Sciences, SRM University AP Andhra Pradesh, Guntur 522502, Andhra Pradesh, India.ORCID 0000-0002-2759-2208
Balázs GulyásLee Kong Chian School of Medicine, Nanyang Technological University Singapore, 59 Nanyang Drive, Singapore 636921, Singapore.
Parasuraman PadmanabhanLee Kong Chian School of Medicine, Nanyang Technological University Singapore, 59 Nanyang Drive, Singapore 636921, Singapore.ORCID 0000-0003-4112-4600
Writoban Basu BallDepartment of Biological Sciences, School of Engineering and Sciences, SRM University AP Andhra Pradesh, Guntur 522502, Andhra Pradesh, India.ORCID 0000-0001-7678-126X

Funding

Department of Science & Technology SRG/2020/001421Science and Engineering Research Board SRG/2020/001421
6 · The paper itself

Abstract

Reactive oxygen species (ROS) contain at least one oxygen atom and one or more unpaired electrons and include singlet oxygen, superoxide anion radical, hydroxyl radical, hydroperoxyl radical, and free nitrogen radicals. Intracellular ROS can be formed as a consequence of several factors, including ultra-violet (UV) radiation, electron leakage during aerobic respiration, inflammatory responses mediated by macrophages, and other external stimuli or stress. The enhanced production of ROS is termed oxidative stress and this leads to cellular damage, such as protein carbonylation, lipid peroxidation, deoxyribonucleic acid (DNA) damage, and base modifications. This damage may manifest in various pathological states, including ageing, cancer, neurological diseases, and metabolic disorders like diabetes. On the other hand, the optimum levels of ROS have been implicated in the regulation of many important physiological processes. For example, the ROS generated in the mitochondria (mitochondrial ROS or mt-ROS), as a byproduct of the electron transport chain (ETC), participate in a plethora of physiological functions, which include ageing, cell growth, cell proliferation, and immune response and regulation. In this current review, we will focus on the mechanisms by which mt-ROS regulate different pathways of host immune responses in the context of infection by bacteria, protozoan parasites, viruses, and fungi. We will also discuss how these pathogens, in turn, modulate mt-ROS to evade host immunity. We will conclude by briefly giving an overview of the potential therapeutic approaches involving mt-ROS in infectious diseases.

Indexed as

MitochondriaReactive Oxygen SpeciesAnimalsHumansImmunityInfectionsOxidative StressReactive Oxygen Speciesbacteriaelectron transport chainfungiinflammasomemitochondrial reactive oxygen speciesprotozoavirus

Identifiers

PMID38927073
PMCPMC11202257

What OpenQuestion holds

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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.