Evidence map›Paper›PMID 39063108›Full record

ReviewInternational journal of molecular sciences2024

Cell Proliferation and Apoptosis-Key Players in the Lung Aging Process.

Jesús Ancer-Rodríguez, Yareth Gopar-Cuevas, Karol García-Aguilar, María-de-Lourdes Chávez-Briones, Ivett Miranda-Maldonado, Adriana Ancer-Arellano, Marta Ortega-Martínez, Gilberto Jaramillo-Rangel

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. β2-Microglobulin Induces Mitochondrial Dysfunction Accompanied by Bronchial Epithelial Cell Senescence.International journal of chronic obstructive pulmonary disease · 2026
    Article
  4. Article
  5. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  6. Article
  7. Article
  8. 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

8 authors.

Jesús Ancer-RodríguezDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
Yareth Gopar-CuevasDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
Karol García-AguilarDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
María-de-Lourdes Chávez-BrionesDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
Ivett Miranda-MaldonadoDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
Adriana Ancer-ArellanoDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
Marta Ortega-MartínezDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.
Gilberto Jaramillo-RangelDepartment of Pathology, School of Medicine, Autonomous University of Nuevo León, Monterrey 64460, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, the global lifespan has increased, resulting in a higher proportion of the population over 65 years. Changes that occur in the lung during aging increase the risk of developing acute and chronic lung diseases, such as acute respiratory distress syndrome, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and lung cancer. During normal tissue homeostasis, cell proliferation and apoptosis create a dynamic balance that constitutes the physiological cell turnover. In basal conditions, the lungs have a low rate of cell turnover compared to other organs. During aging, changes in the rate of cell turnover in the lung are observed. In this work, we review the literature that evaluates the role of molecules involved in cell proliferation and apoptosis in lung aging and in the development of age-related lung diseases. The list of molecules that regulate cell proliferation, apoptosis, or both processes in lung aging includes TNC, FOXM1, DNA-PKcs, MicroRNAs, BCL-W, BCL-XL, TCF21, p16, NOX4, NRF2, MDM4, RPIA, DHEA, and MMP28. However, despite the studies carried out to date, the complete signaling pathways that regulate cell turnover in lung aging are still unknown. More research is needed to understand the changes that lead to the development of age-related lung diseases.

Indexed as

AgingApoptosisCell ProliferationLungAnimalsHumansLung DiseasesSignal Transductionagingapoptosiscell proliferationcell turnoverlunglung diseases

Identifiers

PMID39063108
PMCPMC11276691

What OpenQuestion holds

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Registered trials

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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.