Evidence map›Paper›PMID 36552833›Full record

ArticleCells2022

Histone Citrullination Mediates a Protective Role in Endothelium and Modulates Inflammation.

Rebeca Osca-Verdegal, Jesús Beltrán-García, Ana B Paes, Elena Nacher-Sendra, Susana Novella, Carlos Hermenegildo, Nieves Carbonell, José Luis García-Giménez, Federico V Pallardó

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. Regulation of histones in thromboinflammation.Frontiers in immunology · 2026
    Review
  8. Review
  9. Animals : an open access journal from MDPI · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Proteomics of the heart.Physiological reviews · 2024
    Review
  15. Review
  16. Review
  17. 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

9 authors at 3 institutions in 2 countries.

Rebeca Osca-VerdegalCentro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, 46010 Valencia, Spain.ORCID 0000-0002-0562-5945
Jesús Beltrán-GarcíaDepartment of Medicine, Division of Regenerative Medicine, University of California, La Jolla, CA 92037, USA.ORCID 0000-0002-4292-5509
Ana B PaesDepartamento de Fisiología, Facultad de Medicina y Odontología, Universitat de València, 46010 València, Spain.
Elena Nacher-SendraDepartamento de Fisiología, Facultad de Medicina y Odontología, Universitat de València, 46010 València, Spain.
Susana NovellaDepartamento de Fisiología, Facultad de Medicina y Odontología, Universitat de València, 46010 València, Spain.ORCID 0000-0001-8303-7252
Carlos HermenegildoDepartamento de Fisiología, Facultad de Medicina y Odontología, Universitat de València, 46010 València, Spain.ORCID 0000-0002-4015-2645
Nieves CarbonellInstituto de Investigación Sanitaria INCLIVA, 46010 Valencia, Spain.ORCID 0000-0002-9149-0310
José Luis García-GiménezCentro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, 46010 Valencia, Spain.ORCID 0000-0001-7547-7872
Federico V PallardóCentro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, 46010 Valencia, Spain.ORCID 0000-0003-3715-1980
Universitat de València · ESHospital Clínico Universitario de Valencia · ESSalk Institute for Biological Studies · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NETosis is a key host immune process against a pathogenic infection during innate immune activation, consisting of a neutrophil "explosion" and, consequently, NET formation, containing mainly DNA, histones, and other nuclear proteins. During sepsis, an exacerbated immune host response to an infection occurs, activating the innate immunity and NETosis events, which requires histone H3 citrullination. Our group compared the circulating histone levels with those citrullinated H3 levels in plasma samples of septic patients. In addition, we demonstrated that citrullinated histones were less cytotoxic for endothelial cells than histones without this post-translational modification. Citrullinated histones did not affect cell viability and did not activate oxidative stress. Nevertheless, citrullinated histones induced an inflammatory response, as well as regulatory endothelial mechanisms. Furthermore, septic patients showed elevated levels of circulating citrullinated histone H3, indicating that the histone citrullination is produced during the first stages of sepsis, probably due to the NETosis process.

Indexed as

Extracellular TrapsSepsisCitrullinationEndothelial CellsEndotheliumHistonesHumansInflammationHistonesbiomarkercitrullinationhistonesNETosisprogressionsepsisseptic shock

Identifiers

PMID36552833
PMCPMC9777278
OpenAlexW4312195340

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.