Evidence map›Paper›PMID 39937013›Full record

ReviewCells2025

Update of Aging Hallmarks in Idiopathic Pulmonary Fibrosis.

Ana Lilia Torres-Machorro, Ángeles García-Vicente, Marco Espina-Ordoñez, Erika Luis-García, Miguel Negreros, Iliana Herrera, Carina Becerril, Fernanda Toscano, Jose Cisneros, Mariel Maldonado

Abstract readReview
In one paragraph

Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. mExperimental and therapeutic medicine · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Inflammaging-Driven Osteoporosis: Is a Galectin-Targeted Approach Needed?International journal of molecular sciences · 2025
    Review
  7. 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

10 authors.

Ana Lilia Torres-MachorroLaboratorio de Biología Celular, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.ORCID 0000-0003-3100-6897
Ángeles García-VicenteFacultad de Ciencias, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.
Marco Espina-OrdoñezDepartamento de Investigación en Fibrosis Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.ORCID 0000-0002-7355-6785
Erika Luis-GarcíaLaboratorio de Biología Celular, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.
Miguel NegrerosClínica de Vasculitis Sistémicas Primarias, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.
Iliana HerreraLaboratorio de Biopatología Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.ORCID 0000-0002-4086-7456
Carina BecerrilLaboratorio de Biología Celular, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.
Fernanda ToscanoLaboratorio de Biopatología Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.ORCID 0000-0002-0941-8214
Jose CisnerosDepartamento de Investigación en Fibrosis Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.ORCID 0000-0002-4592-4464
Mariel MaldonadoLaboratorio de Biopatología Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Ciudad de México 14080, Mexico.ORCID 0000-0002-4227-2704

Funding

Consejo Nacional de Humanidades, Ciencias y Tecnologías (CONAHCYT) CF-2023-I-114
6 · The paper itself

Abstract

Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation of fibroblast populations that synthesize large amounts of extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights key findings about IPF characteristics recently recognized as hallmarks of aging, including mechanical alterations, inflammaging, dysbiosis, alternative splicing, and disabled macroautophagy. It also revisits the classic hallmarks of aging, which encompass stem cell exhaustion, cellular senescence, and altered intercellular communication. Enhancing our understanding of the fundamental processes that underlie the altered hallmarks of aging in IPF may facilitate the development of innovative experimental strategies to improve therapeutic outcomes.

Indexed as

AgingIdiopathic Pulmonary FibrosisAnimalsCellular SenescenceHumansaging hallmarksalternative splicingdysbiosisidiopathic pulmonary fibrosisinflammagingmechanical alterations

Identifiers

PMID39937013
PMCPMC11817138

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.