Evidence map›Paper›PMID 31958492›Full record

ReviewExperimental gerontology2020

Cell senescence and fibrotic lung diseases.

Rui-Ming Liu, Gang Liu

Open access · hybridAbstract readReview
In one paragraph

Review in Experimental gerontology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Growth Hormone, Not Simply Just a Hormone for Growth.Endocrinology and metabolism (Seoul, Korea) · 2026
    Review
  5. Article
  6. Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026
    Article
  7. Article
  8. 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
  9. Review
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11 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

2 authors at 1 institution in 1 country.

Rui-Ming LiuDivision of Pulmonary, Allergy, and Critical Care, Department of Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: rliu@uab.edu.
Gang LiuDivision of Pulmonary, Allergy, and Critical Care, Department of Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
University of Alabama at Birmingham · US

Funding

UAB CF Research and Translation Core CenterP30DK072482 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI David M. Bedwell · 2007 to 2026
$23.0M
Program on cellular metabolism and lung fibrosisR35HL135830 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIU, GANG · 2017 to 2023
$5.2M
Glutathione and Lung FibrosisR01HL088141 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIU, RUI-MING · 2008 to 2011
$1.4M
PAI-1 and aging-related susceptibility to lung fibrosisR56HL131054 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIU, RUI-MING · 2016 to 2016
$438k
NHLBI NIH HHS R01 HL088141NHLBI NIH HHS R35 HL135830NHLBI NIH HHS R56 HL131054NIDDK NIH HHS P30 DK072482
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive fatal lung disorder with an unknown etiology and very limited therapeutic options. The incidence and severity of IPF increase with advanced age, suggesting that aging is a major risk factor for IPF. The mechanism underlying the aging-related susceptibility to IPF, however, remains unclear. Cellular senescence, a permanent arrest of cell growth, has been increasingly recognized as an important contributor to aging and aging-related diseases, including IPF. Senescent cells have been identified in IPF lungs and in experimental lung fibrosis models. Removal of senescent cells pharmacologically or genetically improves lung function and reverses pulmonary fibrosis induced by different stimuli in experimental fibrosis models. Treatment with senolytic drugs also improves clinical symptoms in IPF patients. These intriguing findings suggest that cellular senescence contributes importantly to the pathogenesis of fibrotic lung diseases and targeting senescent cells may represent a novel approach for the treatment of fibrotic lung disorders. In this mini review, we summarize the recent advance in the field regarding the role of cellular senescence in fibrotic lung diseases, with a focus on IPF.

Indexed as

Cellular SenescenceAgingFibroblastsHumansIdiopathic Pulmonary FibrosisLungAgingCell senescenceLung fibrosis

Identifiers

PMID31958492
PMCPMC7036279
OpenAlexW3000038289

What OpenQuestion holds

Textmetadata
LicenceTDM
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.