Evidence map›Paper›PMID 31011486›Full record

ArticleAging and disease2019

The Role of Pathological Aging in Cardiac and Pulmonary Fibrosis.

Lucy A Murtha, Matthew Morten, Michael J Schuliga, Nishani S Mabotuwana, Sean A Hardy, David W Waters, Janette K Burgess, Doan Tm Ngo, Aaron L Sverdlov, Darryl A Knight and 1 more

Open access · goldAbstract read
In one paragraph

Article in Aging and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 3 pooled it
5.7field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 95 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Article
  5. mExperimental and therapeutic medicine · 2026
    Review
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  13. GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
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  15. Article
  16. Review
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  19. Article
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5 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

11 authors at 4 institutions in 2 countries.

Lucy A Murtha1School of Medicine and Public Health, The University of Newcastle, Callaghan, NSW, Australia.
Matthew Morten1School of Medicine and Public Health, The University of Newcastle, Callaghan, NSW, Australia.
Michael J Schuliga2School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW, Australia.
Nishani S Mabotuwana1School of Medicine and Public Health, The University of Newcastle, Callaghan, NSW, Australia.
Sean A Hardy1School of Medicine and Public Health, The University of Newcastle, Callaghan, NSW, Australia.
David W Waters2School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW, Australia.
Janette K Burgess4University of Groningen, University Medical Center Groningen, Department of Pathology & Medical Biology, GRIAC (Groningen Research Institute for Asthma and COPD), Groningen and W. J. Kolff Research Institute, The Netherlands.
Doan Tm Ngo2School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW, Australia.
Aaron L Sverdlov1School of Medicine and Public Health, The University of Newcastle, Callaghan, NSW, Australia.
Darryl A Knight2School of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW, Australia.
Andrew J Boyle1School of Medicine and Public Health, The University of Newcastle, Callaghan, NSW, Australia.
Hunter Medical Research Institute · AUUniversity of Newcastle Australia · AUHunter New England Local Health District · AUThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging promotes a range of degenerative pathologies characterized by progressive losses of tissue and/or cellular function. Fibrosis is the hardening, overgrowth and scarring of various tissues characterized by the accumulation of extracellular matrix components. Aging is an important predisposing factor common for fibrotic heart and respiratory disease. Age-related processes such as senescence, inflammaging, autophagy and mitochondrial dysfunction are interconnected biological processes that diminish the regenerative capacity of the aged heart and lung and have been shown to play a crucial role in cardiac fibrosis and idiopathic pulmonary fibrosis. This review focuses on these four processes of aging in relation to their role in fibrosis. It has long been established that the heart and lung are linked both functionally and anatomically when it comes to health and disease, with an ever-expanding aging population, the incidence of fibrotic disease and therefore the number of fibrosis-related deaths will continue to rise. There are currently no feasible therapies to treat the effects of chronic fibrosis therefore highlighting the importance of exploring the processes of aging and its role in inducing and exacerbating fibrosis of each organ. The focus of this review may help to highlight potential avenues of therapeutic exploration.

Indexed as

agingautophagyCardiac fibrosisheartinflammaginglungmitochondrial dysfunctionpulmonary fibrosissenescence

Identifiers

PMID31011486
PMCPMC6457057
OpenAlexW2890443460

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.