Evidence map›Paper›PMID 38397071›Full record

ArticleInternational journal of molecular sciences2024

Pulsed Hyperoxia Acts on Plasmatic Advanced Glycation End Products and Advanced Oxidation Protein Products and Modulates Mitochondrial Biogenesis in Human Peripheral Blood Mononuclear Cells: A Pilot Study on the "Normobaric Oxygen Paradox".

Costantino Balestra, Sara Baldelli, Fabio Virgili, Michele Salvagno, Simona Mrakic-Sposta, Deborah Fratantonio

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
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  5. Review
  6. Article
  7. Normobaric Hyperoxia Therapy in Treating Stroke.Clinical interventions in aging · 2025
    Review
  8. Article
  9. Article
  10. Article
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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 5 institutions in 2 countries.

Costantino BalestraEnvironmental, Occupational, Aging (Integrative) Physiology Laboratory, Haute Ecole Bruxelles-Brabant (HE2B), 1160 Brussels, Belgium.ORCID 0000-0001-6771-839X
Sara BaldelliDepartment of Human Sciences and Promotion of the Quality of Life, IRCCS San Raffaele Pisana, San Raffaele Roma Open University, 00163 Rome, Italy.ORCID 0000-0001-7003-3172
Fabio VirgiliInteruniversitary Consortium "National Institute for Bio-Structures and Bio-Systems"-I.N.B.B., 13, 00136 Rome, Italy.ORCID 0000-0002-9691-8742
Michele SalvagnoDepartment of Intensive Care, Hôpital Universitaire de Bruxelles (HUB), 1070 Brussels, Belgium.ORCID 0000-0002-8415-4247
Simona Mrakic-SpostaInstitute of Clinical Physiology, National Research Council (CNR), 20162 Milan, Italy.ORCID 0000-0001-7359-2690
Deborah FratantonioDepartment of Medicine and Surgery, LUM University, S.S. 100 Km 18, 70100 Casamassima, Italy.ORCID 0000-0003-4835-0571
Istituto Nazionale Biostrutture e Biosistemi · ITLibera Università Maria SS. Assunta · ITNational Research Council · ITSan Raffaele University of Rome · ITUniversité Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The "normobaric oxygen paradox" (NOP) describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as an oxygen shortage, up-regulating redox-sensitive transcription factors. We have previously characterized the time trend of oxygen-sensitive transcription factors in human PBMCs, in which the return to normoxia after 30% oxygen is sensed as a hypoxic trigger, characterized by hypoxia-induced factor (HIF-1) activation. On the contrary, 100% and 140% oxygen induce a shift toward an oxidative stress response, characterized by NRF2 and NF-kB activation in the first 24 h post exposure. Herein, we investigate whether this paradigm triggers Advanced Glycation End products (AGEs) and Advanced Oxidation Protein Products (AOPPs) as circulating biomarkers of oxidative stress. Secondly, we studied if mitochondrial biogenesis was involved to link the cellular response to oxidative stress in human PBMCs. Our results show that AGEs and AOPPs increase in a different manner according to oxygen dose. Mitochondrial levels of peroxiredoxin (PRX3) supported the cellular response to oxidative stress and increased at 24 h after mild hyperoxia, MH (30% O

Indexed as

HyperoxiaOxygenAdvanced Oxidation Protein ProductsGlycation End Products, AdvancedHumansHypoxiaLeukocytes, MononuclearOrganelle BiogenesisOxidative StressPilot ProjectsTranscription FactorsAdvanced Oxidation Protein ProductsGlycation End Products, AdvancedOxygenTranscription Factorshumanmitochondrial biogenesisNrf2oxidative stressperipheral blood mononuclear cells (PBMCs)PGC-1αPrx3reactive oxygen species (ROS)targeted use of oxygen

Identifiers

PMID38397071
PMCPMC10889761
OpenAlexW4391947992

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.