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Clinical and experimental findings have shown that more-severe SAH induces more tenascin-C (TNC) in brain parenchyma, cerebral artery walls, cerebrospinal fluid, and peripheral blood, which is involved in the development of DCI. TNC belongs to inducible, nonstructural, and multifunctional matricellular proteins. TNC is known to regulate multiple signaling pathways and upregulate inflammatory molecules, including some matricellular proteins and the receptors, all of which potentially contribute to the development of DCI with and without cerebral vasospasm. TNC may also form positive feedback mechanisms to induce TNC furthermore, which may lead to the aggravation of DCI at multiple levels. Recently, an antiplatelet drug, cilostazol, and an antiepileptic drug, perampanel, both of which are clinically available and inhibit TNC induction experimentally, were reported to prevent DCI in clinical settings. Many other medications that potentially inhibit TNC upregulation are clinically available. TNC may be promising as a target for intervention in DCI after aneurysmal SAH. Until technological progress develops new TNC-targeting drugs, many already clinically available drugs would be worth repurposing to inhibit TNC induction for the prevention and\/or treatment of DCI after SAH.<\/jats:p>","DOI":"10.1007\/978-3-031-89844-0_2","type":"book-chapter","created":{"date-parts":[[2025,7,10]],"date-time":"2025-07-10T09:45:42Z","timestamp":1752140742000},"page":"11-17","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Tenascin-C as a Target for Intervention in Delayed Cerebral Ischemia After Subarachnoid Hemorrhage"],"prefix":"10.1007","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8555-5448","authenticated-orcid":false,"given":"Hidenori","family":"Suzuki","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumihiro","family":"Kawakita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hideki","family":"Nakajima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroki","family":"Oinaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mai","family":"Nampei","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yume","family":"Suzuki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,7,10]]},"reference":[{"key":"2_CR1","doi-asserted-by":"publisher","first-page":"137","DOI":"10.1093\/neuros\/nyx364","volume":"83","author":"SH Ahn","year":"2018","unstructured":"Ahn SH, Savarraj JP, Pervez M, Jones W, Park J, Jeon SB, Kwon SU, Chang TR, Lee K, Kim DH, Day AL, Choi HA. 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Suzuki reports personal fees from Eisai and Kowa and a research fund from Japan Blood Products Organization outside the submitted work. 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