Evidence map›Paper›PMID 30552558›Full record

ReviewMetabolic brain disease2019

Therapeutic potentials of the Rho kinase inhibitor Fasudil in experimental autoimmune encephalomyelitis and the related mechanisms.

Yuqing Yan, Jiezhong Yu, Ye Gao, Gajendra Kumar, Minfang Guo, Yijin Zhao, Qingli Fang, Huiyu Zhang, Jingwen Yu, Yuqiang Jiang and 2 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 30 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

12 authors at 5 institutions in 3 countries.

Yuqing YanInstitute of Brain Science, Shanxi Datong University, Datong, China.
Jiezhong YuInstitute of Brain Science, Shanxi Datong University, Datong, China.
Ye GaoInstitute of Brain Science, Shanxi Datong University, Datong, China.
Gajendra KumarDepartment of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Minfang GuoInstitute of Brain Science, Shanxi Datong University, Datong, China.
Yijin ZhaoInstitute of Brain Science, Shanxi Datong University, Datong, China.
Qingli FangInstitute of Brain Science, Shanxi Datong University, Datong, China.
Huiyu ZhangInstitute of Brain Science, Shanxi Datong University, Datong, China.
Jingwen YuInstitute of Brain Science, Shanxi Datong University, Datong, China.
Yuqiang JiangState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China. yqjiang@genetics.ac.cn.
Han-Ting ZhangInstitute of Brain Science, Shanxi Datong University, Datong, China. hzhang@hsc.wvu.edu.
Cun-Gen MaInstitute of Brain Science, Shanxi Datong University, Datong, China. macungen2001@163.com.
Shanxi Datong University · CNChinese Academy of Sciences · CNBlanchette Rockefeller Neurosciences Institute · USCity University of Hong Kong · HKInstitute of Genetics and Developmental Biology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS), Parkinson's disease (PD), Alzheimer's disease (AD), and other neurodegenerative diseases of central nervous system (CNS) disorders are serious human health problems. Rho-kinase (ROCK) is emerging as a potentially important therapeutic target relevant to inflammatory neurodegeneration diseases. This is supported by studies showing the beneficial effects of fasudil, a ROCK inhibitor, in inflammatory neurodegeneration diseases. MS is an autoimmune disease resulting from inflammation and demyelination in the white matter of the CNS. It has been postulated that activation of Rho/ROCK causes neuropathological changes accompanied with related clinical symptoms, which are improved by treatment with ROCK inhibitors. Therefore, inhibition of abnormal activation of the Rho/ROCK signaling pathway appears to be a new mechanism for treating CNS diseases. In this review, we extensively discussed the role of ROCK inhibitors, summarized the efficacy of fasudil in the MS conventional animal model of experimental autoimmune encephalomyelitis (EAE), both in vivo and in vitro, and highlighted the mechanism involved. Overall, the findings collected in this review support the role of the ROCK signaling pathway in neurodegenerative diseases. Hence, ROCK inhibitors such as fasudil can be novel, and efficacious treatment for inflammatory neurodegenerative diseases.

Indexed as

1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAnimalsCytokinesEncephalomyelitis, Autoimmune, ExperimentalHumansInflammationMultiple SclerosisProtein Kinase Inhibitorsrho-Associated Kinases1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineCytokinesfasudilProtein Kinase Inhibitorsrho-Associated KinasesExperimental autoimmune encephalomyelitisFasudilMicroglia/macrophagesMultiple sclerosisRho-kinase

Identifiers

PMID30552558
OpenAlexW2904085028

What OpenQuestion holds

Textmetadata
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.