Evidence map›Paper›PMID 32986850›Full record

ArticleBritish journal of pharmacology2020

Rho kinase inhibitor fasudil reduces l-DOPA-induced dyskinesia in a rat model of Parkinson's disease.

Andrea Lopez-Lopez, Carmen M Labandeira, Jose L Labandeira-Garcia, Ana Muñoz

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-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

23 citing papers in PubMed, 38 citations in OpenAlex.

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  3. Fasudil inhibits α-synuclein aggregation through ROCK-inhibition-mediated mechanisms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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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 1 institution in 1 country.

Andrea Lopez-LopezLaboratory of Cellular and Molecular Neurobiology of Parkinson's Disease, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), Department of Morphological Sciences, IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID 0000-0002-1692-9637
Carmen M LabandeiraLaboratory of Cellular and Molecular Neurobiology of Parkinson's Disease, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), Department of Morphological Sciences, IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID 0000-0002-6274-5871
Jose L Labandeira-GarciaLaboratory of Cellular and Molecular Neurobiology of Parkinson's Disease, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), Department of Morphological Sciences, IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID 0000-0002-8243-9791
Ana MuñozLaboratory of Cellular and Molecular Neurobiology of Parkinson's Disease, Research Center for Molecular Medicine and Chronic Diseases (CIMUS), Department of Morphological Sciences, IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID 0000-0002-7214-9774
Universidade de Santiago de Compostela · ES

Funding

Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia ED431C 2018/10Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia ED431G/05European Regional Development FundInstituto de Salud Carlos III RD16/0011/0016Secretaría de Estado de Investigación, Desarrollo e Innovación RTI2018-098830-B-I00
6 · The paper itself

Abstract

background and purposeRho kinase (ROCK) activation is involved in neuroinflammatory processes leading to progression of neurodegenerative diseases such as Parkinson's disease. Furthermore, ROCK plays a major role in angiogenesis. Neuroinflammation and angiogenesis are mechanisms involved in developing l-DOPA-induced dyskinesias (LID). However, it is not known whether ROCK plays a role in LID and whether ROCK inhibitors may be useful against LID. EXPERIMENTAL APPROACH: In rats, we performed short- and long-term dopaminergic lesions using 6-hydroxydopamine and developed a LID model. Effects of dopaminergic lesions and LID on the RhoA/ROCK levels were studied by western blot, real-time PCR analyses and ROCK activity assays in the substantia nigra and striatum. The effects of the ROCK inhibitor fasudil on LID were particularly investigated. KEY

resultsShort-term 6-hydroxydopamine lesions increased nigrostriatal RhoA/ROCK expression, apparently related to the active neuroinflammatory process. However, long-term dopaminergic denervation (completed and stabilized lesions) led to a decrease in RhoA/ROCK levels. Rats with LID showed a significant increase of RhoA and ROCK expression. The development of LID was reduced by the ROCK inhibitor fasudil (10 and 40 mg·kg CONCLUSION AND IMPLICATIONS: The present results suggest that ROCK is involved in the pathophysiology of LID and that ROCK inhibitors such as fasudil may be a novel target for preventing or treating LID. Furthermore, previous studies have revealed neuroprotective effects of ROCK inhibitors.

Indexed as

Dyskinesia, Drug-InducedParkinson Disease1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineAnimalsDisease Models, AnimalLevodopaOxidopamineRatsrho-Associated Kinases1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinefasudilLevodopaOxidopaminerho-Associated KinasesangiogenesisdopamineneuroinflammationnigraParkinsonRhoAROCKstriatum

Identifiers

PMID32986850
PMCPMC7707090
OpenAlexW3090683200

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.