Evidence map›Paper›PMID 40319735›Full record

ArticleRedox biology2025

Differential inflammation, oxidative stress and cardiovascular damage markers of nano- and micro-particle exposure in mice: Implications for human disease burden.

Marin Kuntic, Ivana Kuntic, Dirk Cleppien, Andrea Pozzer, David Nußbaum, Matthias Oelze, Tristan Junglas, Lea Strohm, Henning Ubbens, Steffen Daub and 10 more

Abstract read
In one paragraph

Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Antioxidant Intervention Against Microplastic Hazards.Antioxidants (Basel, Switzerland) · 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

20 authors.

Marin KunticUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.
Ivana KunticUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Dirk CleppienLeibniz Institute for Resilience Research, Mainz, Germany.
Andrea PozzerMax Planck Institute for Chemistry, Atmospheric Chemistry Department, Mainz, Germany.
David NußbaumUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Matthias OelzeUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Tristan JunglasUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Lea StrohmUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Henning UbbensUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Steffen DaubUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Maria Teresa Bayo JimenezUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany.
Sven DanckwardtGerman Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; University Medical Center Ulm, Department of Clinical Chemistry, Ulm, Germany.
Thomas BerkemeierMax Planck Institute for Chemistry, Multiphase Chemistry Department, Mainz, Germany.
Omar HahadUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.
Matthias KohlMax Planck Institute for Chemistry, Atmospheric Chemistry Department, Mainz, Germany.
Sebastian StevenUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; Division of Cardiology, Goethe University Frankfurt, University Hospital, Department of Medicine III, Frankfurt a. M., Germany.
Albrecht StrohLeibniz Institute for Resilience Research, Mainz, Germany; University Medical Center Mainz, Institute of Pathophysiology, Mainz, Germany; Institute of Physiology I, University Hospital Muenster, Germany.
Jos LelieveldMax Planck Institute for Chemistry, Atmospheric Chemistry Department, Mainz, Germany.
Thomas MünzelUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.
Andreas DaiberUniversity Medical Center Mainz, Department for Cardiology 1, Molecular Cardiology, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany; Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg-University, Mainz, Germany. Electronic address: daiber@uni-mainz.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Particulate matter (PM) poses a significant risk to human health; however, it remains uncertain which size fraction is especially harmful and what mechanisms are involved. We investigated the varying effects of particle size on specific organ systems using a custom mouse exposure system and synthetic PM (SPM). Whole-body exposure of mice showed that micrometer-sized fine SPM (2-4 μm) accumulated in the lungs, the primary entry organ, while nanometer-sized SPM (<250 nm) did not accumulate, suggesting a transition into circulation. Mice exposed to micro-SPM exhibited inflammation and NADPH oxidase-derived oxidative stress in the lungs. In contrast, nano-SPM-exposed mice did not display oxidative stress in the lungs but rather at the brain, heart, and vascular levels, supporting the hypothesis that they penetrate the lungs and reach the circulation. Sources of reactive oxygen species from micro-SPM in the lung are NOX1 and NOX2, driven by pulmonary inflammation, while oxidative stress from nano-SPM in the heart is mediated by protein kinase C-dependent p47

Indexed as

Cardiovascular DiseasesInflammationNanoparticlesOxidative StressParticulate MatterAnimalsBiomarkersCardiovascular SystemHumansLungMaleMiceParticle SizeReactive Oxygen SpeciesBiomarkersParticulate MatterReactive Oxygen SpeciesCardiovascular diseaseInflammationOxidative stressSize-dependent effects particulate matterUltrafine particle exposure

Identifiers

PMID40319735
PMCPMC12124686

What Socratic 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 Socratic graph.