{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T22:17:44Z","timestamp":1790201864264,"version":"4.1.0"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,12,19]],"date-time":"2013-12-19T00:00:00Z","timestamp":1387411200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2014,4]]},"abstract":"Summary<\/jats:title>\n \n Background<\/jats:title>\n \n Parkinson's disease (\n PD<\/jats:styled-content>\n ) is a common neurodegenerative disease, characterized by progressive loss of dopaminergic (\n DA<\/jats:styled-content>\n ) neurons in the substantia nigra. Recent investigations have shown that mitochondrial fragmentation, an early event during apoptosis, is implicated in the degeneration of\n DA<\/jats:styled-content>\n neurons in\n PD<\/jats:styled-content>\n , and more importantly, preventing mitochondrial fragmentation could rescue cell death in several\n PD<\/jats:styled-content>\n models. Therefore, mitochondrial dynamics may be a therapeutic target for early intervention in\n PD<\/jats:styled-content>\n . However, much remains unknown about the mechanism underlying mitochondrial fragmentation in\n PD<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n The alterations in mitochondrial morphology, cell apoptosis, and mitochondrial shaping protein levels were detected after\n SH<\/jats:styled-content>\n \u2010\n SY<\/jats:styled-content>\n 5Y cells were treated with various doses of\n MPP<\/jats:styled-content>\n + or rotenone.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Mitochondrial fragmentation is an early event during apoptosis caused by\n MPP<\/jats:styled-content>\n + but not rotenone, and Trichostatin A (\n TSA<\/jats:styled-content>\n ), a commonly used histone deacetylase (\n HDAC<\/jats:styled-content>\n ) inhibitor, selectively rescues mitochondrial fragmentation and cell death induced by lower doses of\n MPP<\/jats:styled-content>\n +. Mitochondrial fragmentation triggered by lower doses of\n MPP<\/jats:styled-content>\n + may be a result of Mfn2 down\u2010regulation, which could be completely reversed by\n TSA<\/jats:styled-content>\n . Further investigation suggests that\n TSA<\/jats:styled-content>\n prevents\n MPP<\/jats:styled-content>\n +\u2010induced Mfn2 down\u2010regulation via inhibiting histone deacetylation over\n Mfn2<\/jats:italic>\n promoter and alleviating its transcriptional dysfunction.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Histone deacetylase inhibitors prevent mitochondrial fragmentation and elicit early neuroprotection in\n PD<\/jats:styled-content>\n cell model induced by\n MPP<\/jats:styled-content>\n +. Hence,\n HDAC<\/jats:styled-content>\n inhibitors may be a potential early treatment for\n PD<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/cns.12217","type":"journal-article","created":{"date-parts":[[2013,12,19]],"date-time":"2013-12-19T03:02:07Z","timestamp":1387422127000},"page":"308-316","source":"Crossref","is-referenced-by-count":52,"title":["Histone Decacetylase Inhibitors Prevent Mitochondrial Fragmentation and Elicit Early Neuroprotection against\n MPP<\/scp>\n +"],"prefix":"10.1111","volume":"20","author":[{"given":"Min","family":"Zhu","sequence":"first","affiliation":[{"name":"Laboratory of Neurology of Integrative Medical Institute Zhongshan Hospital Fudan University Shanghai China"},{"name":"Department of Neurology Institute of Neurology Huashan Hospital Fudan University Shanghai China"},{"name":"The State Key Laboratory of Neurobiology Shanghai Medical College Fudan University Shanghai 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