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Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain
Jiang Q, Shan K, Qun-Wang X, Zhou RM, Yang H, Liu C, Li YJ, Yao J et al.. Oncotarget, 2016-08-01
Topic: Brain proteins, microglia and lab models
Although nervous and vascular systems are functionally different, they usually share similar mechanisms for function maintenance. Neurovascular dysfunction has became the pathogenesis of several vascular and nervous disorders. Here we show that long non-coding RNA-MIAT is aberrantly expressed under neurovascular dysfunction condition. MIAT is shown as a regulator of vascular dysfunction, including retinal angiogenesis, corneal angiogenesis, and vascular permeability. MIAT is also shown as a regulator of retinal neurodegeneration under diabetic condition. Mechanistically, MIAT regulates neural and vascular cell function via MIAT/miR-150-5p/VEGF network. The eye is a valuable model to study central nervous system (CNS) disorders. We show that MIAT knockdown leads to cerebral microvascular degeneration, progressive neuronal loss and neurodegeneration, and behavioral deficits in a CNS neurovascular disorder, Alzheimer's disease. MIAT may represent a pharmacological target for treating neurovascular-related disorders.
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APA 7th
Jiang, Q., Shan, K., Qun-Wang, X., Zhou, R. M., Yang, H., Liu, C., et al. (2016). Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain. Oncotarget. https://doi.org/10.18632/oncotarget.10434
Vancouver
Jiang Q, Shan K, Qun-Wang X, Zhou RM, Yang H, Liu C, et al. Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain. Oncotarget. 2016. doi:10.18632/oncotarget.10434. PMID: 27391072.
BibTeX
@article{jiang2016-27391072,
author = {Jiang, Q. and Shan, K. and Qun-Wang, X. and Zhou, R. M. and Yang, H. and Liu, C. and Li, Y. J. and Yao, J. and others},
title = {{Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain}},
journal = {Oncotarget},
year = {2016},
doi = {10.18632/oncotarget.10434},
pmid = {27391072},
url = {https://doi.org/10.18632/oncotarget.10434}
}
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Key findings
- MIAT is also shown as a regulator of retinal neurodegeneration under diabetic condition.
- Mechanistically, MIAT regulates neural and vascular cell function via MIAT/miR-150-5p/VEGF network.
- The eye is a valuable model to study central nervous system (CNS) disorders.
- We show that MIAT knockdown leads to cerebral microvascular degeneration, progressive neuronal loss and neurodegeneration, and behavioral deficits in a CNS neurovascular disorder, Alzheimer's disease.
- MIAT may represent a pharmacological target for treating neurovascular-related disorders.
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Study details
- Evidence strengthLow
How this study scored 40/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people 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 and multi-centre collaboration, so those were left out: it earned 23 of the 58 points we could judge it on, which is 40 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Oncotarget) |
| 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 | 2016 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| 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 | 2 / 2 | Indexed in PubMed (PMID 27391072) |
| Free to read | 2 / 2 | Free to read |
| Points | 23 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 23 of the 58 points we could judge it on is 40 out of 100. |
| Total | 40 / 100 | — |
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