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dc.rights.licenseopenen_US
dc.contributor.authorABDELAZIZ MOHAMED, Iman
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain-Pierre
dc.contributor.authorHASAN, Anwarul
dc.contributor.authorABDULRAHMAN, Nabeel
dc.contributor.authorMRAICHE, Fatima
dc.date.accessioned2021-04-12T09:40:49Z
dc.date.available2021-04-12T09:40:49Z
dc.date.issued2019-12-03
dc.identifier.issn2073-4409en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/26923
dc.description.abstractEnOsteopontin (OPN) is recognized for its significant roles in both physiological and pathological processes. Initially, OPN was recognized as a cytokine with pro-inflammatory actions. More recently, OPN has emerged as a matricellular protein of the extracellular matrix (ECM). OPN is also known to be a substrate for proteolytic cleavage by several proteases that form an integral part of the ECM. In the adult heart under physiological conditions, basal levels of OPN are expressed. Increased expression of OPN has been correlated with the progression of cardiac remodeling and fibrosis to heart failure and the severity of the condition. The intricate process by which OPN mediates its effects include the coordination of intracellular signals necessary for the differentiation of fibroblasts into myofibroblasts, promoting angiogenesis, wound healing, and tissue regeneration. In this review, we discuss the role of OPN in contributing to the development of cardiac fibrosis and its suitability as a therapeutic target.
dc.language.isoENen_US
dc.subject.enBiomarkers
dc.subject.enCardiomyopathies
dc.subject.enDisease Susceptibility
dc.subject.enFibrosis
dc.subject.enGene Expression Regulation
dc.subject.enHeart Diseases
dc.subject.enHumans
dc.subject.enOsteopontin
dc.subject.enSignal Transduction
dc.title.enOsteopontin: A Promising Therapeutic Target in Cardiac Fibrosis
dc.title.alternativeCellsen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/cells8121558en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologie
dc.identifier.pubmed31816901en_US
bordeaux.journalCellsen_US
bordeaux.volume8en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue12en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.exportfalse
workflow.import.sourcepubmed
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