Evidence map›Paper›PMID 39812558›Full record

ArticleeLife2025

Endocytic recycling is central to circadian collagen fibrillogenesis and disrupted in fibrosis.

Joan Chang, Adam Pickard, Jeremy A Herrera, Sarah O'Keefe, Richa Garva, Matthew Hartshorn, Anna Hoyle, Lewis Dingle, John Knox, Thomas A Jowitt and 10 more

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
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  4. PCPE1 and PCPE2: When Sequence Similarity Masks Functional Diversity.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  5. Article
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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

20 authors.

Joan ChangWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID https://orcid.org/0000-0002-7283-9759
Adam PickardWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Jeremy A HerreraWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Sarah O'KeefeDivision of Molecular and Cellular Function, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Richa GarvaWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID https://orcid.org/0000-0001-7752-8936
Matthew HartshornWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Anna HoyleWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Lewis DingleBlond McIndoe Laboratories, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
John KnoxWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Thomas A JowittWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Madeleine CoyDivision of Molecular and Cellular Function, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID https://orcid.org/0009-0004-7592-861X
Jason WongBlond McIndoe Laboratories, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Adam ReidBlond McIndoe Laboratories, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Yinhui LuWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Cédric ZeltzDepartment of Biomedicine and Centre for Cancer Biomarkers, Norwegian Center of Excellence, University of Bergen, Bergen, Norway.
Rajamiyer V VenkateswaranManchester University National Health Service Foundation Trust, Manchester Academic Health Science Centre, Manchester, United Kingdom.
Patrick T CaswellWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID https://orcid.org/0000-0002-2633-2324
Stephen HighDivision of Molecular and Cellular Function, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.
Donald GullbergDepartment of Biomedicine and Centre for Cancer Biomarkers, Norwegian Center of Excellence, University of Bergen, Bergen, Norway.
Karl E KadlerWellcome Centre for Cell-Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom.ORCID https://orcid.org/0000-0003-4977-4683

Funding

Targeting early events in MUC5B-driven lung injury and fibrosisP01HL162607 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI David Albert Schwartz · 2023 to 2026
$12.4M
Medical Research Council MR/W016796/1Nasjonalföreningen for folkhelsen 16216NHLBI NIH HHS P01 HL162607Norwegian Cancer Society 223052Norwegian Centre of Excellence 223250Wellcome TrustWellcome Trust 110126Wellcome Trust 203128Wellcome Trust 204796Wellcome Trust 204957Wellcome Trust 209741/Z/17/Z
6 · The paper itself

Abstract

Collagen-I fibrillogenesis is crucial to health and development, where dysregulation is a hallmark of fibroproliferative diseases. Here, we show that collagen-I fibril assembly required a functional endocytic system that recycles collagen-I to assemble new fibrils. Endogenous collagen production was not required for fibrillogenesis if exogenous collagen was available, but the circadian-regulated vacuolar protein sorting (VPS) 33b and collagen-binding integrin α11 subunit were crucial to fibrillogenesis. Cells lacking VPS33B secrete soluble collagen-I protomers but were deficient in fibril formation, thus secretion and assembly are separately controlled. Overexpression of VPS33B led to loss of fibril rhythmicity and overabundance of fibrils, which was mediated through integrin α11β1. Endocytic recycling of collagen-I was enhanced in human fibroblasts isolated from idiopathic pulmonary fibrosis, where VPS33B and integrin α11 subunit were overexpressed at the fibrogenic front; this correlation between VPS33B, integrin α11 subunit, and abnormal collagen deposition was also observed in samples from patients with chronic skin wounds. In conclusion, our study showed that circadian-regulated endocytic recycling is central to homeostatic assembly of collagen fibrils and is disrupted in diseases.

Indexed as

Circadian RhythmCollagen Type IEndocytosisFibrosisFibroblastsHumansVesicular Transport ProteinsCollagen Type IVesicular Transport Proteinscell biologycollagenendocytosisfibrillogenesisfibrosishumanintegrinmouse

Identifiers

PMID39812558
PMCPMC11735028

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.