Evidence map›Paper›PMID 37907525›Full record

ArticleNature communications2023

Loss of Grem1-lineage chondrogenic progenitor cells causes osteoarthritis.

Jia Q Ng, Toghrul H Jafarov, Christopher B Little, Tongtong Wang, Abdullah M Ali, Yan Ma, Georgette A Radford, Laura Vrbanac, Mari Ichinose, Samuel Whittle and 12 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.5field-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

29 citing papers in PubMed, 34 citations in OpenAlex.

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  12. Forkhead box O proteins in chondrocyte aging and diseases.Journal of orthopaedic translation · 2025
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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

22 authors at 6 institutions in 2 countries.

Jia Q Ng *Adelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0003-2302-2643
Toghrul H Jafarov *Department of Medicine, Columbia University Medical Center, New York, NY, USA.
Christopher B LittleRaymond Purves Bone & Joint Research Laboratories, Kolling Institute, University of Sydney Faculty of Medicine and Health, Royal North Shore Hospital, St. Leonards, NSW, Australia.ORCID 0000-0002-0353-7634
Tongtong WangAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Abdullah M AliDepartment of Medicine, Columbia University Medical Center, New York, NY, USA.ORCID 0000-0002-4007-6769
Yan MaDepartment of Medicine, Columbia University Medical Center, New York, NY, USA.
Georgette A RadfordAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Laura VrbanacAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Mari IchinoseAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Samuel WhittleAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
David J HunterNorthern Clinical School, University of Sydney, St. Leonards, Sydney, NSW, Australia.ORCID 0000-0003-3197-752X
Tamsin R M LannaganAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Nobumi SuzukiAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Jarrad M GoynePrecision Cancer Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia.
Hiroki KobayashiAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0002-1717-4870
Timothy C WangDepartment of Medicine and Irving Cancer Research Center, Columbia University, New York, NY, USA.
David R HaynesAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Danijela MenicaninAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.
Stan GronthosAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia.ORCID 0000-0002-6225-3084
Daniel L WorthleyPrecision Cancer Medicine Theme, South Australian Health and Medical Research Institute, Adelaide, SA, Australia. dan@colonoscopyclinic.com.au.ORCID 0000-0003-0374-9124
Susan L WoodsAdelaide Medical School, Faculty of Health and Medical Sciences, University of Adelaide, Adelaide, SA, Australia. susan.woods@adelaide.edu.au.ORCID 0000-0002-8955-2017
Siddhartha MukherjeeDepartment of Medicine, Columbia University Medical Center, New York, NY, USA. sm3252@cumc.columbia.edu.ORCID 0000-0001-8251-7334
The University of Adelaide · AUColumbia University Irving Medical Center · USSouth Australian Health and Medical Research Institute · AUCancer Research Center · USThe University of Sydney · AUQueen Elizabeth Hospital · AU

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Anil K Rustgi · 1985 to 2026
$115.3M
Clinical and Translational Science AwardUL1TR001873 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REILLY, MUREDACH P · 2016 to 2025
$99.0M
NCATS NIH HHS UL1 TR001873NCI NIH HHS P30 CA013696
6 · The paper itself

Abstract

Osteoarthritis (OA) is characterised by an irreversible degeneration of articular cartilage. Here we show that the BMP-antagonist Gremlin 1 (Grem1) marks a bipotent chondrogenic and osteogenic progenitor cell population within the articular surface. Notably, these progenitors are depleted by injury-induced OA and increasing age. OA is also caused by ablation of Grem1 cells in mice. Transcriptomic and functional analysis in mice found that articular surface Grem1-lineage cells are dependent on Foxo1 and ablation of Foxo1 in Grem1-lineage cells caused OA. FGFR3 signalling was confirmed as a promising therapeutic pathway by administration of pathway activator, FGF18, resulting in Grem1-lineage chondrocyte progenitor cell proliferation, increased cartilage thickness and reduced OA. These findings suggest that OA, in part, is caused by mechanical, developmental or age-related attrition of Grem1 expressing articular cartilage progenitor cells. These cells, and the FGFR3 signalling pathway that sustains them, may be effective future targets for biological management of OA.

Indexed as

Cartilage, ArticularOsteoarthritisAnimalsCells, CulturedChondrocytesCytokinesGene Expression ProfilingIntercellular Signaling Peptides and ProteinsMiceOsteogenesisStem CellsCytokinesGrem1 protein, mouseIntercellular Signaling Peptides and Proteins

Identifiers

PMID37907525
PMCPMC10618187
OpenAlexW4388078897

What OpenQuestion holds

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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.