Evidence map›Paper›PMID 34209809›Full record

ReviewInternational journal of molecular sciences2021

Cellular Senescence in Lung Fibrosis.

Fernanda Hernandez-Gonzalez, Rosa Faner, Mauricio Rojas, Alvar Agustí, Manuel Serrano, Jacobo Sellarés

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
–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

49 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Hesperetin Alleviates Bleomycin-Induced Pulmonary Fibrosis by Modulating Cellular Senescence and Promoting Impaired Autophagy in a CISD2-Dependent Manner.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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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

6 authors.

Fernanda Hernandez-GonzalezDepartment of Pulmonology, ICR, Hospital Clinic, 08036 Barcelona, Spain.
Rosa FanerInstituto de Investigaciones Biomédicas August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain.
Mauricio RojasDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
Alvar AgustíDepartment of Pulmonology, ICR, Hospital Clinic, 08036 Barcelona, Spain.
Manuel SerranoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology (BIST), 08028 Barcelona, Spain.ORCID 0000-0001-7177-9312
Jacobo SellarésDepartment of Pulmonology, ICR, Hospital Clinic, 08036 Barcelona, Spain.ORCID 0000-0001-5403-5688

Funding

Mapping Age-Related Changes in the LungU01HL145550 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BENOS, PANAGIOTIS V, FINKEL, TOREN · 2019 to 2022
$2.4M
Federación Española de Enfermedades Raras PI17/00369, 452 PI18/1008, PI19/01152Instituto de Salud Carlos III SLT008/18/00176Miguel Servet Research contract CP16/00039NHLBI NIH HHS U01 HL145550
6 · The paper itself

Abstract

Fibrosing interstitial lung diseases (ILDs) are chronic and ultimately fatal age-related lung diseases characterized by the progressive and irreversible accumulation of scar tissue in the lung parenchyma. Over the past years, significant progress has been made in our incomplete understanding of the pathobiology underlying fibrosing ILDs, in particular in relation to diverse age-related processes and cell perturbations that seem to lead to maladaptation to stress and susceptibility to lung fibrosis. Growing evidence suggests that a specific biological phenomenon known as cellular senescence plays an important role in the initiation and progression of pulmonary fibrosis. Cellular senescence is defined as a cell fate decision caused by the accumulation of unrepairable cellular damage and is characterized by an abundant pro-inflammatory and pro-fibrotic secretome. The senescence response has been widely recognized as a beneficial physiological mechanism during development and in tumour suppression. However, recent evidence strengthens the idea that it also drives degenerative processes such as lung fibrosis, most likely by promoting molecular and cellular changes in chronic fibrosing processes. Here, we review how cellular senescence may contribute to lung fibrosis pathobiology, and we highlight current and emerging therapeutic approaches to treat fibrosing ILDs by targeting cellular senescence.

Indexed as

Cellular SenescenceDisease ProgressionFibrosisHumansIdiopathic Pulmonary FibrosisLungLung Diseases, Interstitialagingpulmonary fibrosissenescencesenolyticssenomorphics

Identifiers

PMID34209809
PMCPMC8267738

What OpenQuestion holds

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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.