Evidence map›Paper›PMID 31962055›Full record

ArticleAmerican journal of respiratory cell and molecular biology2020

Impaired Myofibroblast Dedifferentiation Contributes to Nonresolving Fibrosis in Aging.

Kosuke Kato, Naomi J Logsdon, Yoon-Joo Shin, Sunny Palumbo, Adam Knox, Joseph D Irish, Skye P Rounseville, Sydney R Rummel, Mohamed Mohamed, Kareem Ahmad and 5 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.6field-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

59 citing papers in PubMed, 90 citations in OpenAlex.

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  11. Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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  19. Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Kosuke KatoDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Naomi J LogsdonDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Yoon-Joo ShinDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Sunny PalumboDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Adam KnoxDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Joseph D IrishDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Skye P RounsevilleDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Sydney R RummelDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Mohamed MohamedDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Kareem AhmadDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Johnny M TrinhDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Deepali KurundkarDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.
Kenneth S KnoxDivision of Pulmonary and Critical Care Medicine, Department of Medicine, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona.
Victor J ThannickalDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Louise HeckerDivision of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona, Tucson, Arizona.ORCID 0000-0002-5025-5437
University of Arizona · USUniversity of Alabama at Birmingham · US

Funding

Therapeutic Targeting of the Myofibroblast in Fibrotic Lung DiseaseP01HL114470 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THANNICKAL, VICTOR J. · 2013 to 2022
$17.8M
Myofibroblast Senescence in Pulmonary FibrosisR01AG046210 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THANNICKAL, VICTOR J. · 2014 to 2018
$1.6M
Preclinical development of a novel Nrf2-activator formulation for the treatment of idiopathic pulmonary fibrosisR21AG054766 · NIA · UNIVERSITY OF ARIZONA · PI HECKER, LOUISE, MANSOUR, HEIDI M. · 2017 to 2018
$415k
Sirtuins in Lung Aging and FibrosisI01BX003056 · VA · SOUTHEAST LOUISIANA VETERANS HEALTH CARE · PI THANNICKAL, VICTOR J. · 2016 to 2025
–
The role of Nampt in age-associated persistent lung fibrosisI01BX003919 · VA · VETERANS HEALTH ADMINISTRATION · PI HECKER, LOUISE · 2018 to 2022
–
BLRD VA I01 BX003056BLRD VA I01 BX003919NHLBI NIH HHS P01 HL114470NIA NIH HHS R01 AG046210NIA NIH HHS R21 AG054766
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal age-associated disease with no cure. Although IPF is widely regarded as a disease of aging, the cellular mechanisms that contribute to this age-associated predilection remain elusive. In this study, we sought to evaluate the consequences of senescence on myofibroblast cell fate and fibrotic responses to lung injury in the context of aging. We demonstrated that nonsenescent lung myofibroblasts maintained the capacity for dedifferentiation, whereas senescent/IPF myofibroblasts exhibited an impaired capacity for dedifferentiation. We previously demonstrated that the transcription factor MyoD acts as a critical switch in the differentiation and dedifferentiation of myofibroblasts. Here, we demonstrate that decreased levels of MyoD preceded myofibroblast dedifferentiation and apoptosis susceptibility in nonsenescent cells, whereas MyoD expression remained elevated in senescent/IPF myofibroblasts, which failed to undergo dedifferentiation and demonstrated resistance to apoptosis. Genetic strategies to silence MyoD restored the susceptibility of IPF myofibroblasts to undergo apoptosis and led to a partial reversal of age-associated persistent fibrosis

Indexed as

Cell DifferentiationCellular SenescenceAgedAgingAnimalsApoptosisCell LineFemaleFibrosisGene Knockdown TechniquesHumansIdiopathic Pulmonary FibrosisMice, Inbred C57BLMiddle AgedMolecular Targeted TherapyMyoD ProteinMyoD Proteinapoptosis resistanceMyoDmyofibroblast plasticitypulmonary fibrosissenescence

Identifiers

PMID31962055
PMCPMC7193787
OpenAlexW3002131808

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.