Evidence map›Paper›PMID 29247377›Full record

ReviewJournal of cell communication and signaling2018

CCN5/WISP2 and metabolic diseases.

John R Grünberg, Johannes Elvin, Alexandra Paul, Shahram Hedjazifar, Ann Hammarstedt, Ulf Smith

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of cell communication and signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  9. Review
  10. Article
  11. Article
  12. CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023
    Review
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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

6 authors at 3 institutions in 2 countries.

John R GrünbergMetabolic Research Laboratories, Wellcome Trust MRC Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge, CB2 0QQ, UK. jg835@medschl.cam.ac.uk.
Johannes ElvinThe Lundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, the Sahlgrenska Academy, University of Gothenburg, 405 30, Gothenburg, Sweden.
Alexandra PaulDepartment of Biology and Biological Engineering, Chalmers University of Technology, 41296, Gothenburg, Sweden.
Shahram HedjazifarThe Lundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, the Sahlgrenska Academy, University of Gothenburg, 405 30, Gothenburg, Sweden.
Ann HammarstedtThe Lundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, the Sahlgrenska Academy, University of Gothenburg, 405 30, Gothenburg, Sweden.
Ulf SmithThe Lundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, the Sahlgrenska Academy, University of Gothenburg, 405 30, Gothenburg, Sweden.
University of Gothenburg · SEChalmers University of Technology · SEUniversity of Cambridge · GB

Funding

FP7 People: Marie-Curie Actions 608765FP7 Science in Society 607842
6 · The paper itself

Abstract

Obesity and type 2 diabetes increase worldwide at an epidemic rate. It is expected that by the year 2030 around 500 million people will have diabetes; predominantly type 2 diabetes. The CCN family of proteins has become of interest in both metabolic and other common human diseases because of their effects on mesenchymal stem cell (MSCs) proliferation and differentiation as well as being important regulators of fibrosis. We here review current knowledge of the WNT1 inducible signaling pathway protein 2 (CCN5/WISP2). It has been shown to be an important regulator of both these processes through effects on both the canonical WNT and the TGFβ pathways. It is also under normal regulation by the adipogenic commitment factor BMP4, in contrast to conventional canonical WNT ligands, and allows MSCs to undergo normal adipose cell differentiation. CCN5/WISP2 is highly expressed in, and secreted by, MSCs and is an important regulator of MSCs growth. In a transgenic mouse model overexpressing CCN5/WISP2 in the adipose tissue, we have shown that it is secreted and circulating in the blood, the mice develop hypercellular white and brown adipose tissue, have increased lean body mass and enlarged hypercellular hearts. Obese transgenic mice had improved insulin sensitivity. Interestingly, the anti-fibrotic effect of CCN5/WISP2 is protective against heart failure by inhibition of the TGFβ pathway. Understanding how CCN5/WISP2 is regulated and signals is important and may be useful for developing new treatment strategies in obesity and metabolic diseases and it can also be a target in regenerative medicine.

Indexed as

Adipose tissueFibrosisInsulin resistanceMesenchymal stem cellsMetabolismWNT-signaling

Identifiers

PMID29247377
PMCPMC5842198
OpenAlexW2775284846

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.