Evidence map›Paper›PMID 40508111›Full record

ReviewInternational journal of molecular sciences2025

The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.

Daniel Paz-Gomez, Manuel Castillejos-López, Yair Romero, Edgar Flores-Soto, Bianca S Romero-Martinez, Joel Armando Vázquez-Pérez, Georgina Gonzalez-Avila, Victor Ruiz, Ángeles Carlos-Reyes, Rafael Velázquez-Cruz and 7 more

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 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

17 authors.

Daniel Paz-GomezLaboratorio de Investigación en Enfermedades Reumáticas, Instituto Nacional de Enfermedades Respiratorias, Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.
Manuel Castillejos-LópezUnidad de Epidemiología Hospitalaria e Infectología, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0001-8689-9755
Yair RomeroFacultad de Ciencias, Universidad Nacional Autónoma de México (UNAM), Mexico City 04510, Mexico.ORCID 0000-0002-8707-025X
Edgar Flores-SotoDepartamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico City 04510, Mexico.ORCID 0000-0003-2649-8751
Bianca S Romero-MartinezDepartamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico City 04510, Mexico.ORCID 0000-0001-5887-6177
Joel Armando Vázquez-PérezLaboratorio de Biología Molecular de Enfermedades Emergentes y EPOC, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0002-8508-3698
Georgina Gonzalez-AvilaDepartamento de Enfermedades Crónico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0002-3511-4265
Victor RuizLaboratorio de Biología Molecular, Departamento de Fibrosis Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0003-0440-2093
Ángeles Carlos-ReyesLaboratorio de Onco-Inmunobiología, Departamento de Enfermedades Crónico-Degenerativas, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.
Rafael Velázquez-CruzLaboratorio de Genómica del Metabolismo Óseo, Instituto Nacional de Medicina Genómica (INMEGEN), Mexico City 14610, Mexico.ORCID 0000-0003-4515-0777
José Alberto Choreño-ParraFormación de Posgrado, Departamento de Enseñanza, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.
Roberto Lara-LemusDepartamento de Biomedicina Molecular e Investigación Traslacional, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0001-5419-4283
Fausto Rojas-DuranInstituto de Investigaciones del Cerebro, Universidad Veracruzana (UV), Xalapa 91190, Veracruz, Mexico.ORCID 0000-0003-4497-0909
David Martínez BriseñoUnidad de Epidemiología Hospitalaria e Infectología, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0002-8613-2658
Joaquín ZuñigaLaboratorio de Inmunobiología y Genética, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0002-7143-0281
Luz María Torres-EspíndolaLaboratorio de Farmacología, Instituto Nacional de Pediatría (INP), Mexico City 04530, Mexico.ORCID 0000-0001-9929-9361
Arnoldo Aquino-GálvezLaboratorio de Biología Molecular, Departamento de Fibrosis Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.ORCID 0000-0002-2869-5516

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease with limited therapeutic options. This review focuses on the role of retinoids, particularly all-trans retinoic acid (atRA), and hypoxia in the pathogenesis of IPF. Despite an established understanding of genetic and environmental factors in IPF, the interplay between retinoid signaling and the response to hypoxia remains poorly explored due to its complexity. Preclinical evidence suggests that atRA could help reduce pulmonary fibrosis by modulating TGF-β signaling pathways and epithelial-to-mesenchymal transition (EMT). Additionally, we mention other diseases where a relationship between hypoxia and retinoids has been observed. We review how hypoxia, a key factor in the progression of IPF, may influence the efficacy of retinoid therapy. Combination strategies are explored to overcome hypoxia-induced treatment resistance. Finally, we address the complex role of retinoids in lung regeneration, balancing their potential benefits against the risk of exacerbating fibrotic processes. This review suggests that retinoids have potential as a treatment or adjuvant for IPF and highlights the need for further research to elucidate the precise mechanisms of retinoid action in IPF, particularly in hypoxia.

Indexed as

HypoxiaIdiopathic Pulmonary FibrosisRetinoidsAnimalsEpithelial-Mesenchymal TransitionHumansSignal TransductionTretinoinRetinoidsTretinoinall-trans retinoic acid (ATRA)combination therapyhypoxiaidiopathic pulmonary fibrosis (IPF)lung regenerationretinoids

Identifiers

PMID40508111
PMCPMC12154794

What OpenQuestion holds

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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 OpenQuestion graph.