Regulator of G‐protein signalling 5 protects against atherosclerosis in apolipoprotein E‐deficient mice
Wen‐Lin Cheng, Pi‐Xiao Wang, Tao Wang, Yan Zhang, Cheng Du, Hongliang Li, Yong Ji. British Journal of Pharmacology, 2015-01-12
Topic: Inflammation, microglia and astrocytes
Atherosclerotic phenotypes were significantly accelerated in RGS 5 −/− ApoE −/− mice, as indicated by increased inflammatory mediator expression and apoptosis of endothelial cells and macrophages. RGS 5 deficiency enhanced instability of vulnerable plaques by increasing infiltration of macrophages in parallel with the accumulation of lipids, and decreased smooth muscle cell and collagen content. Mechanistically, increased activation of NF ‐ κB and MAPK / ERK 1/2 could be responsible for the accelerated development of atherosclerosis in RGS5‐deficient mice. Conclusions and RGS 5 deletion accelerated development of atherosclerosis and decreased the stability of atherosclerotic plaques partly through activating NF ‐ κB and the MEK‐ERK 1/2 signalling pathways. Linked Articles: This article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-23
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Cheng, W., Wang, P., Wang, T., Zhang, Y., Du, C., Li, H., et al. (2015). Regulator of G‐protein signalling 5 protects against atherosclerosis in apolipoprotein E‐deficient mice. British Journal of Pharmacology. https://doi.org/10.1111/bph.12991
Vancouver
Cheng W, Wang P, Wang T, Zhang Y, Du C, Li H, et al. Regulator of G‐protein signalling 5 protects against atherosclerosis in apolipoprotein E‐deficient mice. British Journal of Pharmacology. 2015. doi:10.1111/bph.12991.
BibTeX
@article{cheng2015-aea781cb,
author = {Cheng, Wen‐Lin and Wang, Pi‐Xiao and Wang, Tao and Zhang, Yan and Du, Cheng and Li, Hongliang and Ji, Yong},
title = {{Regulator of G‐protein signalling 5 protects against atherosclerosis in apolipoprotein E‐deficient mice}},
journal = {British Journal of Pharmacology},
year = {2015},
doi = {10.1111/bph.12991},
url = {https://doi.org/10.1111/bph.12991}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Atherosclerotic phenotypes were significantly accelerated in RGS 5 −/− ApoE −/− mice, as indicated by increased inflammatory mediator expression and apoptosis of endothelial cells and macrophages.
- RGS 5 deficiency enhanced instability of vulnerable plaques by increasing infiltration of macrophages in parallel with the accumulation of lipids, and decreased smooth muscle cell and collagen content.
- Mechanistically, increased activation of NF ‐ κB and MAPK / ERK 1/2 could be responsible for the accelerated development of atherosclerosis in RGS5‐deficient mice.
- Conclusions and RGS 5 deletion accelerated development of atherosclerosis and decreased the stability of atherosclerotic plaques partly through activating NF ‐ κB and the MEK‐ERK 1/2 signalling pathways.
- Linked Articles: This article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 20 of the 56 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (British Journal of Pharmacology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2015 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mice”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 20 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 20 of the 56 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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