Evidence map›Paper›PMID 27391072›Full record

ArticleOncotarget2016

Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain.

Qin Jiang, Kun Shan, Xiao Qun-Wang, Rong-Mei Zhou, Hong Yang, Chang Liu, Yu-Jie Li, Jin Yao, Xiu-Miao Li, Yi Shen and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Non-coding RNA research · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Long Non-Coding RNAs in Retinal Ganglion Cell Apoptosis.Cellular and molecular neurobiology · 2023
    Review
  17. Review
  18. Review
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 1 country.

Qin JiangEye Hospital, Nanjing Medical University, Nanjing, China.
Kun ShanEye Hospital, Nanjing Medical University, Nanjing, China.
Xiao Qun-WangEye Hospital, Nanjing Medical University, Nanjing, China.
Rong-Mei ZhouEye Hospital, Nanjing Medical University, Nanjing, China.
Hong YangEye Hospital, Nanjing Medical University, Nanjing, China.
Chang LiuEye Hospital, Nanjing Medical University, Nanjing, China.
Yu-Jie LiEye Hospital, Nanjing Medical University, Nanjing, China.
Jin YaoEye Hospital, Nanjing Medical University, Nanjing, China.
Xiu-Miao LiEye Hospital, Nanjing Medical University, Nanjing, China.
Yi ShenEye Hospital, Nanjing Medical University, Nanjing, China.
Hong ChengDepartment of Neurology, Jiangsu Province Hospital, Nanjing, China.
Jun YuanDepartment of Neurology, Jiangsu Chinese Medicine Hospital, Nanjing, China.
Yang-Yang ZhangDepartment of Cardiac Surgery, The First School of Clinical Medicine, Nanjing Medical University, Nanjing, China.
Biao YanResearch Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Nanjing Medical University · CNEye & ENT Hospital of Fudan University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Neovascularization, PathologicVascular RemodelingAlzheimer DiseaseAnimalsBrainCentral Nervous System DiseasesDiabetes Mellitus, ExperimentalDisease Models, AnimalMaleMaze LearningMiceMice, Inbred C57BLMicrocirculationNeurodegenerative DiseasesNeurogliaRetinaMiat long non-coding RNARNA, Long Noncodingangiogenesislong non-coding RNAneurodegenerationreactive glia

Identifiers

PMID27391072
PMCPMC5226539
OpenAlexW2472478751

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.