Evidence map›Paper›PMID 32369955›Full record

ReviewBiomolecules2020

Soluble Epoxide Hydrolase Inhibition to Face Neuroinflammation in Parkinson's Disease: A New Therapeutic Strategy.

Mercè Pallàs, Santiago Vázquez, Coral Sanfeliu, Carles Galdeano, Christian Griñán-Ferré

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. The Roles of EETs in Neurological Disorders.CNS neuroscience & therapeutics · 2026
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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

5 authors at 2 institutions in 1 country.

Mercè PallàsPharmacology Section, Department of Pharmacology, Toxicology, and Therapeutic Chemistry. Faculty of Pharmacy and Food Sciences. Institute of Neuroscience, University of Barcelona (NeuroUB), Av. Joan XXIII 27-31, 08028 Barcelona, Spain.ORCID 0000-0003-3095-4254
Santiago VázquezLaboratori de Química Farmacèutica (Unitat Associada al CSIC), Department de Farmacologia, Toxicologia i Química Terapèutica, Facultat de Farmàcia i Ciències de l'Alimentació, and Institute of Biomedicine (IBUB), Universitat de Barcelona, Av. Joan XXIII, 27-31, 08028 Barcelona, Spain.ORCID 0000-0002-9296-6026
Coral SanfeliuInstitut d'Investigacions Biomèdiques de Barcelona (IIBB), CSIC, IDIBAPS and CIBERESP, C/ Roselló 161, 08036 Barcelona, Spain.
Carles GaldeanoDepartment of Pharmacy and Pharmaceutical Technology and Physical Chemistry, Faculty of Pharmacy and Food Sciences and Institute of Biomedicine (IBUB), University of Barcelona, Av. Joan XXIII, 27-31, 08028 Barcelona, Spain.ORCID 0000-0003-1702-0369
Christian Griñán-FerréPharmacology Section, Department of Pharmacology, Toxicology, and Therapeutic Chemistry. Faculty of Pharmacy and Food Sciences. Institute of Neuroscience, University of Barcelona (NeuroUB), Av. Joan XXIII 27-31, 08028 Barcelona, Spain.ORCID 0000-0002-5424-9130
Universitat de Barcelona · ESCentro de Investigación Biomédica en Red · ES

Funding

Generalitat de Catalunya 2017 SGR 106Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2016-77703Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2017-82771-R
6 · The paper itself

Abstract

Neuroinflammation is a crucial process associated with the pathogenesis of neurodegenerative diseases, including Parkinson's disease (PD). Several pieces of evidence suggest an active role of lipid mediators, especially epoxy-fatty acids (EpFAs), in the genesis and control of neuroinflammation; 14,15-epoxyeicosatrienoic acid (14,15-EET) is one of the most commonly studied EpFAs, with anti-inflammatory properties. Soluble epoxide hydrolase (sEH) is implicated in the hydrolysis of 14,15-EET to its corresponding diol, which lacks anti-inflammatory properties. Preventing EET degradation thus increases its concentration in the brain through sEH inhibition, which represents a novel pharmacological approach to foster the reduction of neuroinflammation and by end neurodegeneration. Recently, it has been shown that sEH levels increase in brains of PD patients. Moreover, the pharmacological inhibition of the hydrolase domain of the enzyme or the use of sEH knockout mice reduced the deleterious effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration. This paper overviews the knowledge of sEH and EETs in PD and the importance of blocking its hydrolytic activity, degrading EETs in PD physiopathology. We focus on imperative neuroinflammation participation in the neurodegenerative process in PD and the putative therapeutic role for sEH inhibitors. In this review, we also describe highlights in the general knowledge of the role of sEH in the central nervous system (CNS) and its participation in neurodegeneration. We conclude that sEH is one of the most promising therapeutic strategies for PD and other neurodegenerative diseases with chronic inflammation process, providing new insights into the crucial role of sEH in PD pathophysiology as well as a singular opportunity for drug development.

Indexed as

8,11,14-Eicosatrienoic AcidAnimalsAnti-Inflammatory AgentsBrainEnzyme InhibitorsEpoxide HydrolasesHumansNeuroprotective AgentsParkinson Disease14,15-epoxy-5,8,11-eicosatrienoic acid8,11,14-Eicosatrienoic AcidAnti-Inflammatory AgentsEnzyme InhibitorsEpoxide HydrolasesNeuroprotective Agentsepoxyeicosatrienoic acidsneurodegenerationneuroinflammationParkinson’s diseasesoluble epoxide hydrolase

Identifiers

PMID32369955
PMCPMC7277900
OpenAlexW3022775719

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.