{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T08:07:48Z","timestamp":1790755668887,"version":"4.1.0"},"reference-count":49,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,6,21]],"date-time":"2019-06-21T00:00:00Z","timestamp":1561075200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003407","name":"Ministero dell\u2019Istruzione, dell\u2019Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003407","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Introduction<\/jats:italic>: The molecular mechanism of immune\u2010mediated necrotizing myopathy (IMNM) remains unknown. Autophagy impairment, described in autoimmune diseases, is a key process in myofiber protein degradation flux and muscle integrity and has not been studied in IMNM.<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>: Muscle biopsies from patients with IMNM (<jats:italic>n<\/jats:italic> = 40), dermatomyositis (DM; 24), polymyositis (PM; 8), polymyositis with mitochondrial pathology (4), sporadic inclusion body myositis (8), and controls (6) were compared by immunohistochemistry.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>: The proportions of myofibers containing autophagy markers LC3b and p62 were higher in IMNM than in DM or PM and correlated with creatine kinase levels. In IMNM, compartmentalized LC3b puncta were located in regenerating and degenerating myofibers surrounded by major histocompatibility complex type II<jats:sup>+<\/jats:sup> inflammatory cells. Several IMNM myofibers accumulated ubiquitin and misfolded protein.<\/jats:p><jats:p><jats:italic>Discussion<\/jats:italic>: The detection of LC3b<jats:sup>+<\/jats:sup> or p62<jats:sup>+<\/jats:sup> myofibers could be used in differentiating IMNM from PM. The identification of autophagy\u2010modifying molecules potentially could improve patients\u2019 outcomes. <jats:italic>Muscle Nerve<\/jats:italic>, 2019<\/jats:p>","DOI":"10.1002\/mus.26608","type":"journal-article","created":{"date-parts":[[2019,6,7]],"date-time":"2019-06-07T06:55:07Z","timestamp":1559890507000},"page":"315-327","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["Autophagy markers LC3 and p62 accumulate in immune\u2010mediated necrotizing myopathy"],"prefix":"10.1002","volume":"60","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8706-3386","authenticated-orcid":false,"given":"Francesco","family":"Girolamo","sequence":"first","affiliation":[{"name":"Unit of Human Anatomy and Histology, Department of Basic Medical Sciences, Neuroscience and Sense Organs  Bari 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