{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,26]],"date-time":"2025-10-26T21:16:17Z","timestamp":1761513377711},"reference-count":46,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,11,17]],"date-time":"2013-11-17T00:00:00Z","timestamp":1384646400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The identification of new components implicated in the pathogenesis of osteoarthritis (<jats:styled-content style=\"fixed-case\">OA<\/jats:styled-content>) might improve our understanding of the disease process. Here, we investigated the levels of the survival of motor neuron (<jats:styled-content style=\"fixed-case\">SMN<\/jats:styled-content>) expression in <jats:styled-content style=\"fixed-case\">OA<\/jats:styled-content> cartilage considering the fundamental role of the <jats:styled-content style=\"fixed-case\">SMN<\/jats:styled-content> protein in cell survival and its involvement in other stress\u2010associated pathologies. We report that <jats:styled-content style=\"fixed-case\">SMN<\/jats:styled-content> expression is up\u2010regulated in human <jats:styled-content style=\"fixed-case\">OA<\/jats:styled-content> compared with normal cartilage, showing a strong correlation with the disease severity, a result confirmed <jats:italic>in vivo<\/jats:italic> in an experimental model of the disease. We further show that the prominent inflammatory cytokines (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1) are critical inducers of <jats:styled-content style=\"fixed-case\">SMN<\/jats:styled-content> expression. This is in marked contrast with the reported impaired levels of <jats:styled-content style=\"fixed-case\">SMN<\/jats:styled-content> in spinal muscular atrophy, a single inherited neuromuscular disorder characterized by mutations in the <jats:italic>smn<\/jats:italic> gene whereas <jats:styled-content style=\"fixed-case\">OA<\/jats:styled-content> is a complex disease with multiple aetiologies. While the precise functions of <jats:styled-content style=\"fixed-case\">SMN<\/jats:styled-content> during <jats:styled-content style=\"fixed-case\">OA<\/jats:styled-content> remain to be elucidated, the conclusions of this study shed light on a novel pathophysiological pathway involved in the progression of <jats:styled-content style=\"fixed-case\">OA<\/jats:styled-content>, potentially offering new targets for therapy.<\/jats:p>","DOI":"10.1111\/jcmm.12170","type":"journal-article","created":{"date-parts":[[2013,11,18]],"date-time":"2013-11-18T02:33:04Z","timestamp":1384741984000},"page":"115-124","source":"Crossref","is-referenced-by-count":9,"title":["Enhanced expression of the central survival of motor neuron (<scp>SMN<\/scp>) protein during the pathogenesis of osteoarthritis"],"prefix":"10.1111","volume":"18","author":[{"given":"Magali","family":"Cucchiarini","sequence":"first","affiliation":[{"name":"Center of Experimental Orthopaedics Saarland University Medical Center 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