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dc.contributor.authorKiyoshi Kikuchien_US
dc.contributor.authorHisaaki Uchikadoen_US
dc.contributor.authorNaohisa Miyagien_US
dc.contributor.authorYoko Morimotoen_US
dc.contributor.authorIto Takashien_US
dc.contributor.authorSalunya Tancharoenen_US
dc.contributor.authorNaoki Miuraen_US
dc.contributor.authorKie Miyataen_US
dc.contributor.authorRokudai Sakamotoen_US
dc.contributor.authorChiemi Kikuchien_US
dc.contributor.authorNarumi Iidaen_US
dc.contributor.authorNaoto Shiomien_US
dc.contributor.authorTerukazu Kuramotoen_US
dc.contributor.authorK. Ichi Kawaharaen_US
dc.contributor.otherYame Public Hospitalen_US
dc.contributor.otherKurume University School of Medicineen_US
dc.contributor.otherKagoshima University Faculty of Medicineen_US
dc.contributor.otherMahidol Universityen_US
dc.contributor.otherKagoshima Universityen_US
dc.contributor.otherNishida Koutoku Hospitalen_US
dc.contributor.otherKohjin Co., Ltd.en_US
dc.contributor.otherSaiseikai Shiga Hospitalen_US
dc.contributor.otherOmuta City General Hospitalen_US
dc.date.accessioned2018-05-03T07:58:57Z-
dc.date.available2018-05-03T07:58:57Z-
dc.date.issued2011-12-01en_US
dc.identifier.citationInternational Journal of Molecular Medicine. Vol.28, No.6 (2011), 899-906en_US
dc.identifier.issn1791244Xen_US
dc.identifier.issn11073756en_US
dc.identifier.other2-s2.0-80053510027en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=80053510027&origin=inwarden_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/11423-
dc.description.abstractFree radicals play major roles in the pathogenesis of tissue damage in many diseases and clinical conditions, and the removal of free radicals may offer a treatment option. Several modulators of free radical scavenger pathways have been developed and some have progressed to clinical trials. One such agent, edaravone, was approved in 2001 in Japan for the treatment of cerebral infarction. It has since been shown that edaravone can diffuse into many organs and, in addition to its effects on hydroxyl radical removal, edaravone modulates inflammatory processes, matrix metalloproteinase levels, nitric oxide production, apoptotic cell death, and necrotic cell death. Edaravone also exerts protective effects in a number of animal models of disease and tissue damage, including models of myocardial, lung, intestinal, liver, pancreatic and renal injury. Together with the proven safety of edaravone following 9 years of use as a modulator of free radical scavenging pathways in neurological disease, these additional effects of edaravone suggest that it may offer a novel treatment for several non-neurological diseases and clinical conditions in humans.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=80053510027&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleBeyond neurological disease: New targets for edaravone (Review)en_US
dc.typeReviewen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.3892/ijmm.2011.795en_US
Appears in Collections:Scopus 2011-2015

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