Evidence map›Paper›PMID 37458437›Full record

ReviewAmerican journal of physiology. Cell physiology2023

Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis.

Tanyalak Parimon, Peter Chen, Barry R Stripp, Jiurong Liang, Dianhua Jiang, Paul W Noble, William C Parks, Changfu Yao

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
18.1field-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

56 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Combatting pulmonary fibrosis withChinese herbal medicines · 2026
    Review
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  8. Review
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  10. Review
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  14. Review
  15. Article
  16. Review
  17. Article
  18. Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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  20. 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 at 1 institution in 1 country.

Tanyalak ParimonDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.ORCID 0000-0002-4790-0730
Peter ChenDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.ORCID 0000-0002-5330-1718
Barry R StrippDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.ORCID 0000-0003-4348-2137
Jiurong LiangDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.
Dianhua JiangDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.
Paul W NobleDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.
William C ParksDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.
Changfu YaoDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States.
Cedars-Sinai Medical Center · US

Funding

UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
Role of Surfactant Proteins in Mediating Noninfectious Inflammatory and FibroproP01HL108793 · NHLBI · DUKE UNIVERSITY · PI NOBLE, PAUL WESLEY · 2012 to 2022
$21.3M
The Effect of Nanoparticle Encapsulated Resveratrol on Treatment of PeriodontitisKL2TR001882 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Elizabeta Nemeth · 2016 to 2026
$13.1M
Molecular Regulation of Progressive Pulmonary FibrosisR35HL150829 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Paul Wesley Noble · 2020 to 2026
$5.7M
ZIP8-dependent Zinc Metabolic Regulation in Alveolar Progenitor Cell Aging and FibrosisR01AG078655 · NIA · CEDARS-SINAI MEDICAL CENTER · PI Carol Jiurong Liang, Paul Wesley Noble · 2022 to 2026
$2.7M
Syndecan-1 suppression of lung inflammation - Diversity SupplementR01HL159953 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI CHEN, PETER · 2022 to 2025
$2.7M
Fungal dysbiosis regulation of post-influenza bacterial pneumoniaR01HL155759 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI CHEN, PETER · 2021 to 2024
$2.4M
Dynactin 4 regulation of lung injuryR01HL137076 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI CHEN, PETER, SCHROER, TRINA A · 2018 to 2021
$1.9M
Syndecan-1 regulation of lung fibrosisK08HL141590 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI PARIMON, TANYALAK · 2020 to 2024
$854k
A Patient-Specific hiPSC Model of Nilotinib-Induced Peripheral Artery Disease PharmacogenomicsF31HL151160 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PINHEIRO, EMILY · 2020 to 2022
$129k
NCATS NIH HHS KL2 TR001882NCATS NIH HHS UL1 TR001881NHLBI NIH HHS F31 HL151160NHLBI NIH HHS K08 HL141590NHLBI NIH HHS P01 HL108793NHLBI NIH HHS R01 HL137076NHLBI NIH HHS R01 HL155759NHLBI NIH HHS R01 HL159953NHLBI NIH HHS R35 HL150829NIA NIH HHS R01 AG078655
6 · The paper itself

Abstract

Pulmonary fibrosis comprises a range of chronic interstitial lung diseases (ILDs) that impose a significant burden on patients and public health. Among these, idiopathic pulmonary fibrosis (IPF), a disease of aging, is the most common and most severe form of ILD and is treated largely by lung transplantation. The lack of effective treatments to stop or reverse lung fibrosis-in fact, fibrosis in most organs-has sparked the need to understand causative mechanisms with the goal of identifying critical points for potential therapeutic intervention. Findings from many groups have indicated that repeated injury to the alveolar epithelium-where gas exchange occurs-leads to stem cell exhaustion and impaired alveolar repair that, in turn, triggers the onset and progression of fibrosis. Cellular senescence of alveolar epithelial progenitors is a critical cause of stemness failure. Hence, senescence impairs repair and thus contributes significantly to fibrosis. In this review, we discuss recent evidence indicating that senescence of epithelial progenitor cells impairs alveolar homeostasis and repair creating a profibrotic environment. Moreover, we discuss the impact of senescent alveolar epithelial progenitors, alveolar type 2 (AT2) cells, and AT2-derived transitional epithelial cells in fibrosis. Emerging evidence indicates that transitional epithelial cells are prone to senescence and, hence, are a new player involved in senescence-associated lung fibrosis. Understanding the complex interplay of cell types and cellular regulatory factors contributing to alveolar epithelial progenitor senescence will be crucial to developing targeted therapies to mitigate their downstream profibrotic sequelae and to promote normal alveolar repair.

Indexed as

Alveolar Epithelial CellsIdiopathic Pulmonary FibrosisAgedAgingCellular SenescenceEpithelial CellsHumansLungStem Cellsepithelial cellsfibrosisprogenitor cellsSASPsenescence

Identifiers

PMID37458437
PMCPMC10511168
OpenAlexW4384523363

What OpenQuestion holds

Textmetadata
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.