{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T22:17:47Z","timestamp":1790201867875,"version":"4.1.0"},"reference-count":42,"publisher":"SAGE Publications","issue":"11","license":[{"start":{"date-parts":[[2016,10,1]],"date-time":"2016-10-01T00:00:00Z","timestamp":1475280000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2016,10]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Aims:<\/jats:italic>\n                    <\/jats:bold>\n                    Dysfunctional regulation of mitochondrial dynamics, which switches the balance to fission, is involved in neurodegeneration in Parkinson's disease (PD). Dynamin-related protein-1 (Drp1), a key regulator of mitochondrial fission, has been attributed recently to such neurodegeneration in PD. However, the machinery that connects Drp1 to the pathophysiology of PD is unclear.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Results:<\/jats:italic>\n                    <\/jats:bold>\n                    We demonstrated that nitric oxide (NO) was overproduced on 1-methyl-4-phenylpyridinium ion (MPP\n                    <jats:sup>+<\/jats:sup>\n                    ) treatment, which subsequently engendered S-nitrosylation of Parkin (SNO-Parkin), and thus decreased the interaction with Drp1, leading to elevated Drp1 expression. Consistent with this, Drp1 was elevated in the ventral midbrain of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated PD mouse models, a region usually affected by PD. Concomitantly, in a mouse model of MPTP-induced PD, both SNO-Parkin and Drp1 levels were increased, whereas no significant difference in SNO-Drp1 protein levels were found in these mice. In addition, NO stress, induced by MPP\n                    <jats:sup>+<\/jats:sup>\n                    , triggered the phosphorylation of Drp1 Ser616 and caused its subsequent recruitment to the mitochondria. These events create a death-prone environment that contributes to the loss of dopaminergic neurons.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Innovation:<\/jats:italic>\n                    <\/jats:bold>\n                    We first showed that SNO-Parkin reduced its ability as a suppressor of Drp1 expression, leading to upregulation of Drp1 in neurotoxin-based PD models,\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    .\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic>\n                    <\/jats:bold>\n                    Our results provide a molecular explanation for the contribution of Drp1 to the pathogenesis of sporadic PD. These findings indicate that the SNO-Parkin pathway may be a novel therapeutic target to treat PD.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal<\/jats:italic>\n                    . 25, 609\u2013622.\n                  <\/jats:p>","DOI":"10.1089\/ars.2016.6634","type":"journal-article","created":{"date-parts":[[2016,6,7]],"date-time":"2016-06-07T23:52:45Z","timestamp":1465343565000},"page":"609-622","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":72,"title":["The Essential Role of Drp1 and Its Regulation by S-Nitrosylation of Parkin in Dopaminergic Neurodegeneration: Implications for Parkinson's Disease"],"prefix":"10.1177","volume":"25","author":[{"given":"Zhenzhen","family":"Zhang","sequence":"first","affiliation":[{"name":"South China Normal University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Liu","sequence":"additional","affiliation":[{"name":"South China Normal University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"XiaoXiao","family":"Jiang","sequence":"additional","affiliation":[{"name":"South China Normal University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ShaoDong","family":"Zhai","sequence":"additional","affiliation":[{"name":"South China Normal University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Da","family":"Xing","sequence":"additional","affiliation":[{"name":"South China Normal University","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2016,10,10]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.emboj.7601253"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2009.03.006"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0808249105"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.06.010"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1171091"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1093891"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(03)00568-3"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0719-07.2007"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.expneurol.2009.05.027"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200802164"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2012.4928"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/nprot.2006.342"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1002\/ana.10483"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00222.2006"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2417"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymeth.2008.09.018"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1038\/70978"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2011.03.042"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2015.6334"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1089\/ars.2011.4019"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.0918-13.2013"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1186\/1750-1326-6-34"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.200809125"},{"key":"e_1_3_3_25_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0709336105"},{"key":"e_1_3_3_26_2","first-page":"83","article-title":"Free radical and nitric oxide toxicity in Parkinson's disease","volume":"91","author":"Przedborski S","year":"2003","unstructured":"Przedborski S, , Jackson-Lewis V, , Vila M, , Wu DC, , Teismann P, , Tieu K, , Choi DK, , and Cohen O. 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