Evidence map›Paper›PMID 30497529›Full record

ReviewClinical epigenetics2018

Noncoding RNAs in multiple sclerosis.

Xuan Yang, Yuzhang Wu, Bei Zhang, Bing Ni

Open access · goldAbstract readReview
In one paragraph

Review in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 76 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Xuan YangDepartment of Immunology, Medical College of Qingdao University, 308 Ningxia Road, Shinan District, Qingdao, 266003, China.
Yuzhang WuInstitute of Immunology of PLA, Third Military Medical University, 30 Gaotanyan St., Shapingba District, Chongqing, 400038, China.
Bei ZhangDepartment of Immunology, Medical College of Qingdao University, 308 Ningxia Road, Shinan District, Qingdao, 266003, China. 914054186@qq.com.
Bing NiDepartment of Pathophysiology, Third Military Medical University, 30 Gaotanyan St., Shapingba District, Chongqing, 400038, China. nibingxi@126.com.ORCID 0000-0002-4297-5346
Army Medical University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS), a chronic inflammatory demyelinating disease of the central nervous system, is characterized by axonal degeneration and gliosis. Although the causes of MS remain unknown, gene dysregulation in the central nervous system has been associated with the disease pathogenesis. As such, the various regulators of gene expression may be contributing factors. The noncoding (nc) RNAs have piqued the interest of MS researchers due to their known functions in human physiology and various pathological processes, despite being generally characterized as transcripts without apparent protein-coding capacity. Accumulating evidence has indicated that ncRNAs participate in the regulation of MS by acting as epigenetic factors, especially the long (l) ncRNAs and the micro (mi) RNAs, and they are now recognized as key regulatory molecules in MS. In this review, we summarize the most current studies on the contribution of ncRNAs in MS pathogenic processes and discuss their potential applications in the diagnosis and treatment of MS.

Indexed as

AnimalsEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansMicroRNAsMultiple SclerosisRNA, Long NoncodingMicroRNAsRNA, Long NoncodingcircRNAslncRNAsmiRNAsMultiple sclerosisncRNAs

Identifiers

PMID30497529
PMCPMC6267072
OpenAlexW2903426398

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.