Evidence map›Paper›PMID 42072674›Full record

ReviewBiomolecules2026

The Role of Neutrophil, Monocyte and Macrophage Calprotectin and S100A12 in the Fibrotic Process.

Nora Elemi Regino-Zamarripa, Ana Sofía Burciaga, Moisés Bocanegra-Mondragón, Alfredo Cruz-Lagunas, Ángel Camarena, Luis Jiménez-Alvarez, Remedios Ramírez, Gustavo Ramírez-Martínez, Joaquín Zúñiga

Abstract readReview
In one paragraph

Review in Biomolecules, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Nora Elemi Regino-ZamarripaLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.
Ana Sofía BurciagaLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.
Moisés Bocanegra-MondragónLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.
Alfredo Cruz-LagunasLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.
Ángel CamarenaLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.
Luis Jiménez-AlvarezLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.
Remedios RamírezFacultad de Ciencias, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Gustavo Ramírez-MartínezLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.ORCID 0000-0001-5157-0677
Joaquín ZúñigaLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico.ORCID 0000-0002-7143-0281

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is a progressive and irreversible mechanism affecting any organ. During tissue injury, fibroblast activation is necessary for wound healing but the uncontrolled accumulation of fibrotic tissue leads to local organ damage. The fibrotic process involves the excessive accumulation of extracellular matrix components and inflammatory mediators. Since sustained inflammation precedes fibrosis, the involvement of immune cells, like neutrophils, monocytes and macrophages, is crucial to elucidate its pathogenesis. These immune cells release proinflammatory cytokines and chemokines, and also proteins that act as fibroblast proliferation mediators, such as the S100/calgranulins subgroup, comprising S100A8, S100A9, and S100A12 proteins. Moreover, a homodimer of S100A8 binds to a homodimer of S100A9 forming the heterodimer S100A8/A9, called calprotectin, which is abundant in the cytosol of neutrophils during immune activation. Although calprotectin (S100A8/A9) is the most predominant form, calgranulins S100A8 and S100A9 have independent functions of calprotectin (S100A8/9) complex formation. These calcium-binding proteins have proinflammatory functions and are potential inflammation biomarkers. More evidence in different fibrosis disorders highlights their role as relevant fibroblast proliferation mediators and prognosis markers. Hence, this review focuses on the current understanding of the role of S100A8, S100A9, and S100A12 calgranulins and calprotectin (S100A8/A9) in the fibrotic process of different disorders, and their potential application as disease severity and prognosis biomarkers.

Indexed as

FibrosisLeukocyte L1 Antigen ComplexMacrophagesMonocytesNeutrophilsS100A12 ProteinAnimalsHumansLeukocyte L1 Antigen ComplexS100A12 ProteinS100A12 protein, humancalgranulinscalprotectin (S100A8/A9)fibrosismacrophagesmonocytesneutrophilsproinflammatory processS100 proteins

Identifiers

PMID42072674
PMCPMC13114093

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.