| Title |
CCN5/WISP2 and metabolic diseases
|
|---|---|
| Published in |
Journal of Cell Communication and Signaling, December 2017
|
| DOI | 10.1007/s12079-017-0437-z |
| Pubmed ID | |
| Authors |
John R Grünberg, Johannes Elvin, Alexandra Paul, Shahram Hedjazifar, Ann Hammarstedt, Ulf Smith |
| 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. |
X Demographics
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Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 30 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 5 | 17% |
| Student > Bachelor | 4 | 13% |
| Researcher | 3 | 10% |
| Student > Master | 3 | 10% |
| Student > Postgraduate | 3 | 10% |
| Other | 2 | 7% |
| Unknown | 10 | 33% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 11 | 37% |
| Medicine and Dentistry | 3 | 10% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 3% |
| Neuroscience | 1 | 3% |
| Chemistry | 1 | 3% |
| Other | 1 | 3% |
| Unknown | 12 | 40% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 December 2017.
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#20,456,235
of 23,012,811 outputs
Outputs from Journal of Cell Communication and Signaling
#211
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#375,105
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Outputs of similar age from Journal of Cell Communication and Signaling
#12
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