Evidence map›Paper›PMID 28883924›Full record

ArticleBMJ open respiratory research2017

Metabolic heterogeneity of idiopathic pulmonary fibrosis: a metabolomic study.

Yidan D Zhao, Li Yin, Stephen Archer, Catherine Lu, George Zhao, Yan Yao, Licun Wu, Michael Hsin, Thomas K Waddell, Shaf Keshavjee and 2 more

Abstract read
In one paragraph

Article in BMJ open respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

140 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Advances in metabolic reprogramming of pulmonary fibrosis.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
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  7. Article
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  16. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  17. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  18. Review
  19. Article
  20. Article

80 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

12 authors.

Yidan D ZhaoDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Li YinDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Stephen ArcherDepartment of Medicine, Queen's University, Kingston, Ontario, Canada.
Catherine LuDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
George ZhaoDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Yan YaoDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Licun WuDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Michael HsinDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Thomas K WaddellDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
Shaf KeshavjeeDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.
John GrantonDivision of Respirology, University Health Network, Toronto, Ontario, Canada.
Marc de PerrotDepartment of Thoracic Surgery, University Health Network, Toronto, Ontario, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIdiopathic pulmonary fibrosis (IPF) is a chronic and fatal disease of unknown cause characterised by progressive fibrotic formation in lung tissue. We hypothesise that disrupted metabolic pathways in IPF contribute to disease pathogenesis.

methodsMetabolomics of human IPF was performed using mass spectroscopy (IPF lung=8; donor lung=8). Gene expression of key metabolic enzymes was measured using microarrays. Of the 108 metabolites whose levels were found altered, 48 were significantly increased, whereas 60 were significantly decreased in IPF samples compared with normal controls.

resultsSpecific metabolic pathways mediating the IPF remodelling were found with a downregulated sphingolipid metabolic pathway but an upregulated arginine pathway in IPF. In addition, disrupted glycolysis, mitochondrial beta-oxidation and tricarboxylic acid cycle, altered bile acid, haem and glutamate/aspartate metabolism were found in IPF samples compared with control.

conclusionsOur results show alterations in metabolic pathways for energy consumption during lung structural remodelling, which may contribute to IPF pathogenesis. We believe that this is the first report of simultaneously and systemically measuring changes of metabolites involving nine metabolic pathways in human severe IPF lungs. The measurement of the metabolites may serve in the future diagnosis and prognosis of IPF.

Indexed as

interstitial fibrosislung transplantation

Identifiers

PMID28883924
PMCPMC5531310

What OpenQuestion holds

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Registered trials

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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.