{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T12:24:10Z","timestamp":1792153450625,"version":"4.4.0"},"reference-count":33,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,10,11]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Stroke is a leading cause of long\u2010term disability worldwide. However, current therapies that promote functional recovery from stroke are limited to physical rehabilitation. No pharmacological therapy is available. Thus, understanding the role of histone deacetylase 2 (HDAC2) in the pathophysiological process of stroke\u2010induced functional loss may provide a novel strategy for stroke recovery.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Focal stroke was induced by photothrombosis. LV\u2010HDAC2\u2010shRNA\u2010GFP, LV\u2010GFP, Ad\u2010HDAC2\u2010Flag, or Ad\u2010inactive\u2010HDAC2\u2010Flag was microinjected into the peri\u2010infarct area immediately after stroke. HDAC inhibitors were microinjected into the peri\u2010infarct area 4 to 10\u00a0days after stroke. Grid\u2010walking task and cylinder task were conducted to assess motor function. Golgi\u2010Cox staining, chromatin immunoprecipitation, and electrophysiology were used to reveal the mechanisms underlying stroke recovery. Knockdown or knockout of HDAC2 promoted stroke recovery, whereas overexpression of HDAC2 worsened stroke\u2010induced functional impairment. More importantly, trichostatin A, a pan\u2010HDAC inhibitor, promoted functional recovery from stroke in WT mice when used in the delayed phase, but it was ineffective in\n                      <jats:italic>Hdac2<\/jats:italic>\n                      conditional knockout (\n                      <jats:italic>Hdac2<\/jats:italic>\n                      CKO) mice. Treatment with suberoylanilide hydroxamic acid, a selective HDAC1 and HDAC2 inhibitor, in the delayed phase of stroke produced sustained functional recovery in mice via epigenetically enhancing neuroplasticity of surviving neurons in the peri\u2010infarct zone.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Our novel findings provide evidence that HDAC2 is a crucial target for functional recovery from stroke. As there are clinically available HDAC inhibitors, our findings could be directly translated into clinical research of stroke.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.117.007236","type":"journal-article","created":{"date-parts":[[2017,10,5]],"date-time":"2017-10-05T20:10:26Z","timestamp":1507234226000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":67,"title":["Inhibiting Histone Deacetylase 2 (HDAC2) Promotes Functional Recovery From Stroke"],"prefix":"10.1161","volume":"6","author":[{"given":"Ying","family":"Tang","sequence":"first","affiliation":[{"name":"Institution of Stem Cells and Neuroregeneration, School of Pharmacy, Nanjing Medical University, Nanjing, China"},{"name":"Department of Pharmacology, School of Pharmacy, Nanjing Medical University, Nanjing, 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