Evidence map›Paper›PMID 39919729›Full record

ArticleRespirology (Carlton, Vic.)2025

Pre-Treatment MMP7 Predicts Progressive Idiopathic Pulmonary Fibrosis in Antifibrotic Treated Patients.

Roger M Li, Dino B A Tan, Chantalia Tedja, Wendy A Cooper, Helen E Jo, Christopher Grainge, Ian N Glaspole, Nicole Goh, Samantha Ellis, Peter M A Hopkins and 10 more

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In one paragraph

Article in Respirology (Carlton, Vic.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
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  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Roger M LiInstitute for Respiratory Health, Nedlands, Western Australia, Australia.
Dino B A TanInstitute for Respiratory Health, Nedlands, Western Australia, Australia.ORCID 0000-0001-9108-2360
Chantalia TedjaInstitute for Respiratory Health, Nedlands, Western Australia, Australia.
Wendy A CooperRoyal Prince Alfred Hospital, Sydney, New South Wales, Australia.
Helen E JoCentre of Research Excellence in Pulmonary Fibrosis, Sydney, NSW, Australia.
Christopher GraingeCentre of Research Excellence in Pulmonary Fibrosis, Sydney, NSW, Australia.ORCID 0000-0002-6565-9928
Ian N GlaspoleCentre of Research Excellence in Pulmonary Fibrosis, Sydney, NSW, Australia.ORCID 0000-0002-5118-2890
Nicole GohCentre of Research Excellence in Pulmonary Fibrosis, Sydney, NSW, Australia.ORCID 0000-0003-2065-4346
Samantha EllisThe Alfred Hospital, Melbourne, Victoria, Australia.
Peter M A HopkinsUniversity of Queensland, St Lucia, Queensland, Australia.
Christopher ZappalaUniversity of Queensland, St Lucia, Queensland, Australia.
Gregory J KeirUniversity of Queensland, St Lucia, Queensland, Australia.ORCID 0000-0001-9979-8726
Paul N ReynoldsCentre of Research Excellence in Pulmonary Fibrosis, Sydney, NSW, Australia.ORCID 0000-0002-2273-1774
Sally ChapmanRoyal Adelaide Hospital, Adelaide, South Australia, Australia.ORCID 0000-0002-9310-7258
E Haydn WaltersUniversity of Melbourne, Melbourne, Victoria, Australia.
Darryl KnightProvidence Health Care Research Institute, Vancouver, British Columbia, Canada.ORCID 0000-0002-4064-6127
Svetlana BalticUniversity of Western Australia, Crawley, Western Australia, Australia.
HuiJun ChihCurtin University, Bentley, Western Australia, Australia.
Tamera J CorteCentre of Research Excellence in Pulmonary Fibrosis, Sydney, NSW, Australia.ORCID 0000-0002-7096-9365
Yuben P MoodleyInstitute for Respiratory Health, Nedlands, Western Australia, Australia.ORCID 0000-0002-0777-1196

Funding

Boehringer IngelheimLung Foundation AustraliaNational Health and Medical Research Council GNT1116371National Health and Medical Research Council GNT2015613
6 · The paper itself

Abstract

BACKGROUND AND

objectiveIdiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease with a poor prognosis. Antifibrotics slow the decline of pulmonary function after 12-months, but limited studies have examined the role of circulatory biomarkers in antifibrotic treated IPF patients.

methodsSerum from 98 IPF participants, from the Australian Idiopathic Pulmonary Fibrosis Registry were collected at four time-points over 1 year post-antifibrotic treatment and analysed as two separate cohorts. Patients were stratified as progressive, if they experienced ≥ 10% decline in FVC or ≥ 15% decline in DLCO or were deceased within 1 year of treatment initiation: or otherwise as stable. Ten molecules of interest were measured by ELISAs in patient serum.

resultsBaseline MMP7 levels were higher in progressive than stable patients in Cohort 1 (p = 0.02) and Cohort 2 (p = 0.0002). Baseline MMP7 levels also best differentiated progressive from stable patients (Cohort 1, AUC = 0.74, p = 0.02; Cohort 2, AUC = 0.81, p = 0.0003). Regression analysis of the combined cohort showed that elevated MMP7 levels predicted 12-month progression (OR = 1.530, p = 0.010) and increased risk of overall mortality (HR = 1.268, p = 0.002). LASSO regression identified a multi-biomarker panel (MMP7, ICAM-1, CHI3L1, CA125) that differentiated progression more accurately than MMP7 alone. Furthermore, GAP combined with MMP7, ICAM-1, CCL18 and SP-D was more predictive of 3-year mortality than GAP alone.

conclusionMMP7 along with a multi-biomarker and GAP panel can predict IPF progression and mortality, with the potential for optimising management.

Indexed as

Antifibrotic AgentsIdiopathic Pulmonary FibrosisMatrix Metalloproteinase 7AgedAustraliaBiomarkersCohort StudiesDisease ProgressionFemaleHumansMaleMiddle AgedPrognosisRegistriesAntifibrotic AgentsBiomarkersMatrix Metalloproteinase 7MMP7 protein, humanbiomarkerdisease progressionidiopathic pulmonary fibrosis

Identifiers

PMID39919729
PMCPMC12128705

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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.