{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T17:23:15Z","timestamp":1787764995990,"version":"build-2784847793"},"reference-count":59,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:p>JOURNAL\/nrgr\/04.03\/01300535-202411000-00028\/figure1\/v\/2026-06-18T063637Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>\n                    Calcium influx into neurons triggers neuronal death during cerebral ischemia\/reperfusion injury. Various calcium channels are involved in cerebral ischemia\/reperfusion injury. Cav3.2 channel is a main subtype of T-type calcium channels. T-type calcium channel blockers, such as pimozide and mibefradil, have been shown to prevent cerebral ischemia\/reperfusion injury-induced brain injury. However, the role of Cav3.2 channels in cerebral ischemia\/reperfusion injury remains unclear. Here,\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    models of cerebral ischemia\/reperfusion injury were established using middle cerebral artery occlusion in mice and high glucose hypoxia\/reoxygenation exposure in primary hippocampal neurons. The results showed that Cav3.2 expression was significantly upregulated in injured hippocampal tissue and primary hippocampal neurons. We further established a Cav3.2 gene-knockout mouse model of cerebral ischemia\/reperfusion injury. Cav3.2 knockout markedly reduced infarct volume and brain water content, and alleviated neurological dysfunction after cerebral ischemia\/reperfusion injury. Additionally, Cav3.2 knockout attenuated cerebral ischemia\/reperfusion injury-induced oxidative stress, inflammatory response, and neuronal apoptosis. In the hippocampus of Cav3.2-knockout mice, calcineurin overexpression offset the beneficial effect of Cav3.2 knockout after cerebral ischemia\/reperfusion injury. These findings suggest that the neuroprotective function of Cav3.2 knockout is mediated by calcineurin\/nuclear factor of activated T cells 3 signaling. Findings from this study suggest that Cav3.2 could be a promising target for treatment of cerebral ischemia\/reperfusion injury.\n                  <\/jats:p>","DOI":"10.4103\/1673-5374.390966","type":"journal-article","created":{"date-parts":[[2023,12,14]],"date-time":"2023-12-14T09:08:28Z","timestamp":1702544908000},"page":"2480-2487","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":27,"title":["Cav3.2 channel regulates cerebral ischemia\/reperfusion injury: a promising target for intervention"],"prefix":"10.4103","volume":"19","author":[{"given":"Feibiao","family":"Dai","sequence":"first","affiliation":[{"name":"Graduate School, Wannan Medical College, Wuhu, Anhui Province, China"},{"name":"Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui Province, China"},{"name":"Core Facility Center for Medical 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