Evidence map›Paper›PMID 34207528›Full record

ReviewInternational journal of molecular sciences2021

Cellular Senescence: Pathogenic Mechanisms in Lung Fibrosis.

Tanyalak Parimon, Miriam S Hohmann, Changfu Yao

Open access · goldAbstract 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 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
10.7field-weighted citation impact, top 1% of its field
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

72 citing papers in PubMed, 114 citations in OpenAlex.

  1. Review
  2. Review
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  4. Article
  5. Review
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  9. Article
  10. Article
  11. Review
  12. Article
  13. Integrating mechanical cues inFrontiers in immunology · 2026
    Review
  14. Article
  15. Article
  16. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  17. Article
  18. 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
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Tanyalak ParimonCedars-Sinai Medical Center, Department of Medicine, Women's Guild Lung Institute, Los Angeles, CA 90048, USA.ORCID 0000-0002-4790-0730
Miriam S HohmannCedars-Sinai Medical Center, Department of Medicine, Women's Guild Lung Institute, Los Angeles, CA 90048, USA.ORCID 0000-0003-2667-3919
Changfu YaoCedars-Sinai Medical Center, Department of Medicine, Women's Guild Lung Institute, Los Angeles, CA 90048, USA.
Cedars-Sinai Medical Center · US

Funding

The Effect of Nanoparticle Encapsulated Resveratrol on Treatment of PeriodontitisKL2TR001882 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Elizabeta Nemeth · 2016 to 2026
$13.1M
Syndecan-1 regulation of lung fibrosisK08HL141590 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI PARIMON, TANYALAK · 2020 to 2024
$854k
NCATS NIH HHS KL2 TR001882NHLBI NIH HHS K08 HL141590NIH HHS K08 HL141590-01A1NIH HHS NCATS KL2TR001882
6 · The paper itself

Abstract

Pulmonary fibrosis is a chronic and fatal lung disease that significantly impacts the aging population globally. To date, anti-fibrotic, immunosuppressive, and other adjunct therapy demonstrate limited efficacies. Advancing our understanding of the pathogenic mechanisms of lung fibrosis will provide a future path for the cure. Cellular senescence has gained substantial interest in recent decades due to the increased incidence of fibroproliferative lung diseases in the older age group. Furthermore, the pathologic state of cellular senescence that includes maladaptive tissue repair, decreased regeneration, and chronic inflammation resembles key features of progressive lung fibrosis. This review describes regulatory pathways of cellular senescence and discusses the current knowledge on the senescence of critical cellular players of lung fibrosis, including epithelial cells (alveolar type 2 cells, basal cells, etc.), fibroblasts, and immune cells, their phenotypic changes, and the cellular and molecular mechanisms by which these cells contribute to the pathogenesis of pulmonary fibrosis. A few challenges in the field include establishing appropriate in vivo experimental models and identifying senescence-targeted signaling molecules and specific therapies to target senescent cells, known collectively as "senolytic" or "senotherapeutic" agents.

Indexed as

Cellular SenescenceSignal TransductionAlveolar Epithelial CellsAnimalsDisease Models, AnimalFibroblastsHumansIdiopathic Pulmonary Fibrosiscellular senescencelung fibrosispathogenesis

Identifiers

PMID34207528
PMCPMC8227105
OpenAlexW3170910701

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.