{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T03:26:48Z","timestamp":1792985208770,"version":"4.5.0"},"reference-count":42,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2015,12,29]],"date-time":"2015-12-29T00:00:00Z","timestamp":1451347200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Korean Health Technology R&D Project, Ministry of Health & Welfare","award":["HI14C18070000"],"award-info":[{"award-number":["HI14C18070000"]}],"id":[{"id":"https:\/\/ror.org\/00vxgjw72","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:p>\n                    As lysosomal hydrolysis has long been suggested to be responsible for myelin clearance after peripheral nerve injury, in this study, we investigated the possible role of autophagolysosome formation in myelin phagocytosis by Schwann cells and its final contribution to nerve regeneration. We found that the canonical formation of autophagolysosomes was induced in demyelinating Schwann cells after injury, and the inhibition of autophagy via Schwann cell\u2010specific knockout of the\n                    <jats:italic>atg7<\/jats:italic>\n                    gene or pharmacological intervention of lysosomal function caused a significant delay in myelin clearance. However, Schwann cell dedifferentiation, as demonstrated by extracellular signal\u2010regulated kinase activation and c\u2010Jun induction, and redifferentiation were not significantly affected, and thus the entire repair program progressed normally in\n                    <jats:italic>atg7<\/jats:italic>\n                    knockout mice. Finally, autophagic Schwann cells were also found during segmental demyelination in a mouse model of inflammatory peripheral neuropathy. Together, our findings suggest that autophagy is the self\u2010myelin destruction mechanism of Schwann cells, but mechanistically, it is a process distinct from Schwann cell plasticity for nerve repair. GLIA 2016;64:730\u2013742\n                  <\/jats:p>","DOI":"10.1002\/glia.22957","type":"journal-article","created":{"date-parts":[[2015,12,29]],"date-time":"2015-12-29T06:03:30Z","timestamp":1451369010000},"page":"730-742","source":"Crossref","is-referenced-by-count":145,"title":["Autophagic myelin destruction by schwann cells during wallerian degeneration and segmental demyelination"],"prefix":"10.1002","volume":"64","author":[{"given":"So Young","family":"Jang","sequence":"first","affiliation":[{"name":"Department of Physiology Mitochondria Hub Regulation Center, Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoon Kyung","family":"Shin","sequence":"additional","affiliation":[{"name":"Department of Physiology Mitochondria Hub Regulation Center, Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"So Young","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Mitochondria Hub Regulation Center, Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joo Youn","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Physiology Mitochondria Hub Regulation Center, Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye Jeong","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Mitochondria Hub Regulation Center, Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young Hyun","family":"Yoo","sequence":"additional","affiliation":[{"name":"Department of Anatomy Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jong Kuk","family":"Kim","sequence":"additional","affiliation":[{"name":"Neurology, College of Medicine Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hwan Tae","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Physiology Mitochondria Hub Regulation Center, Dong\u2010a University Busan Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,12,29]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2012.06.021"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00691081"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1749-6632.1999.tb08574.x"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1186\/1742-2094-8-110"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.15-10-06445.1995"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.201503019"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/glia.22796"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3766-04.2005"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7600309"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.27.3.651"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0116624"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1002\/glia.20761"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneurpsyc.1950.02310250111010"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4537-10.2011"},{"key":"e_1_2_6_16_1","doi-asserted-by":"crossref","unstructured":"KleinD PatzkoA SchreiberD vanHauwermeirenA BaierM GrohJ WestBL MartiniR.2015. 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