Evidence map›Paper›PMID 29594387›Full record

ReviewCellular and molecular life sciences : CMLS2018

Redox-dependent thiol modifications: implications for the release of extracellular vesicles.

Birke J Benedikter, Antje R Weseler, Emiel F M Wouters, Paul H M Savelkoul, Gernot G U Rohde, Frank R M Stassen

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
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  7. Review
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  9. Article
  10. Article
  11. Review
  12. Article
  13. The Redox Enzyme Thioredoxin Is Increased in Plasma Extracellular Vesicles From Endurance-Trained Females in Response to Acute Exercise.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Extracellular Vesicles for Disease Treatment.International journal of nanomedicine · 2025
    Review
  18. Review
  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 at 4 institutions in 3 countries.

Birke J BenedikterDepartment of Medical Microbiology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.ORCID http://orcid.org/0000-0002-1103-2484
Antje R WeselerDepartment of Pharmacology and Toxicology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, PO Box 616, 6200 MD, Maastricht, The Netherlands.ORCID http://orcid.org/0000-0002-2862-0186
Emiel F M WoutersDepartment of Respiratory Medicine, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
Paul H M SavelkoulDepartment of Medical Microbiology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, PO Box 5800, 6202 AZ, Maastricht, The Netherlands.
Gernot G U RohdeMedical Clinic I, Department of Respiratory Medicine, Goethe University Hospital, Frankfurt/Main, Germany.ORCID http://orcid.org/0000-0002-5193-7755
Frank R M StassenDepartment of Medical Microbiology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center, PO Box 5800, 6202 AZ, Maastricht, The Netherlands. f.stassen@maastrichtuniversity.nl.
University Medical Center · USGoethe University Frankfurt · DEMaastricht University · NLMaastricht University Medical Centre · NL

Funding

Nederlandse Organisatie voor Wetenschappelijk Onderzoek 022.003.011
6 · The paper itself

Abstract

Extracellular vesicles (EVs), including microvesicles and exosomes, are emerging as important regulators of homeostasis and pathophysiology. During pro-inflammatory and pro-oxidant conditions, EV release is induced. As EVs released under such conditions often exert pro-inflammatory and procoagulant effects, they may actively promote the pathogenesis of chronic diseases. There is evidence that thiol group-containing antioxidants can prevent EV induction by pro-inflammatory and oxidative stimuli, likely by protecting protein thiols of the EV-secreting cells from oxidation. As the redox state of protein thiols greatly impacts three-dimensional protein structure and, consequently, function, redox modifications of protein thiols may directly modulate EV release in response to changes in the cell's redox environment. In this review article, we discuss targets of redox-dependent thiol modifications that are known or expected to be involved in the regulation of EV release, namely redox-sensitive calcium channels, N-ethylmaleimide sensitive factor, protein disulfide isomerase, phospholipid flippases, actin filaments, calpains and cell surface-exposed thiols. Thiol protection is proposed as a strategy for preventing detrimental changes in EV signaling in response to inflammation and oxidative stress. Identification of the thiol-containing proteins that modulate EV release in pro-oxidant environments could provide a rationale for broad application of thiol group-containing antioxidants in chronic inflammatory diseases.

Indexed as

AntioxidantsExtracellular VesiclesHumansInflammationOxidation-ReductionSignal TransductionSulfhydryl CompoundsAntioxidantsSulfhydryl CompoundsChronic inflammationExosomesMicrovesiclesN-acetyl-L-cysteineRedox environmentSulfhydryl groups

Identifiers

PMID29594387
PMCPMC5986851
OpenAlexW2794836997

What OpenQuestion holds

Textmetadata
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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.