Evidence map›Paper›PMID 37869014›Full record

ArticleFrontiers in immunology2023

Pia M Vornewald, Ruth Forman, Rouan Yao, Naveen Parmar, Håvard T Lindholm, Lilith S K Lee, Mara Martín-Alonso, Kathryn J Else, Menno J Oudhoff

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 4 institutions in 3 countries.

Pia M VornewaldCEMIR - Center of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, Trondheim, Norway.
Ruth FormanLydia Becker Institute of Immunology & Inflammation, School of Biological Sciences, The University of Manchester, Manchester, United Kingdom.
Rouan YaoCEMIR - Center of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, Trondheim, Norway.
Naveen ParmarCEMIR - Center of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, Trondheim, Norway.
Håvard T LindholmPrincess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
Lilith S K LeeCEMIR - Center of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, Trondheim, Norway.
Mara Martín-AlonsoCEMIR - Center of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, Trondheim, Norway.
Kathryn J ElseLydia Becker Institute of Immunology & Inflammation, School of Biological Sciences, The University of Manchester, Manchester, United Kingdom.
Menno J OudhoffCEMIR - Center of Molecular Inflammation Research, Department of Clinical and Molecular Medicine, NTNU - Norwegian University of Science and Technology, Trondheim, Norway.
Norwegian University of Science and Technology · NOUniversity of Manchester · GBCarleton University · CAUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal epithelial homeostasis is maintained by intrinsic and extrinsic signals. The extrinsic signals include those provided by mesenchymal cell populations that surround intestinal crypts and is further facilitated by the extracellular matrix (ECM), which is modulated by proteases such as matrix metalloproteinases (MMPs). Extrinsic signals ensure an appropriate balance between intestinal epithelial proliferation and differentiation. This study explores the role of MMP17, which is preferentially expressed by smooth muscle cells in the intestine, in intestinal homeostasis and during immunity to infection. Mice lacking MMP17 expressed high levels of goblet-cell associated genes and proteins, such as CLCA1 and RELM-β, which are normally associated with immune responses to infection. Nevertheless,

Indexed as

Matrix Metalloproteinase 17TrichuriasisAnimalsColonGoblet CellsMatrix Metalloproteinases, Membrane-AssociatedMicePersistent InfectionTrichurisMatrix Metalloproteinase 17Matrix Metalloproteinases, Membrane-AssociatedMmp17 protein, mouseCitrobacter rodentiumgoblet cellhelminthintestinal immunitymatrix metalloproteinases (MMPs)MMP17niche factorTrichuris muris

Identifiers

PMID37869014
PMCPMC10587605
OpenAlexW4387402784

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.