{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T16:44:09Z","timestamp":1793724249410,"version":"4.6.1"},"reference-count":54,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"700","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Transl. Med."],"published-print":{"date-parts":[[2023,6,14]]},"abstract":"<jats:p>Intracranial aneurysms (IAs) are a high-risk factor for life-threatening subarachnoid hemorrhage. Their etiology, however, remains mostly unknown at present. We conducted screening for sporadic somatic mutations in 65 IA tissues (54 saccular and 11 fusiform aneurysms) and paired blood samples by whole-exome and targeted deep sequencing. We identified sporadic mutations in multiple signaling genes and examined their impact on downstream signaling pathways and gene expression in vitro and an arterial dilatation model in mice in vivo. We identified 16 genes that were mutated in at least one IA case and found that these mutations were highly prevalent (92%: 60 of 65 IAs) among all IA cases examined. In particular, mutations in six genes (<jats:italic>PDGFRB<\/jats:italic>,<jats:italic>AHNAK<\/jats:italic>,<jats:italic>OBSCN<\/jats:italic>,<jats:italic>RBM10<\/jats:italic>,<jats:italic>CACNA1E<\/jats:italic>, and<jats:italic>OR5P3<\/jats:italic>), many of which are linked to NF-\u03baB signaling, were found in both fusiform and saccular IAs at a high prevalence (43% of all IA cases examined). We found that mutant PDGFRBs constitutively activated ERK and NF-\u03baB signaling, enhanced cell motility, and induced inflammation-related gene expression in vitro. Spatial transcriptomics also detected similar changes in vessels from patients with IA. Furthermore, virus-mediated overexpression of a mutant<jats:italic>PDGFRB<\/jats:italic>induced a fusiform-like dilatation of the basilar artery in mice, which was blocked by systemic administration of the tyrosine kinase inhibitor sunitinib. Collectively, this study reveals a high prevalence of somatic mutations in NF-\u03baB signaling pathway\u2013related genes in both fusiform and saccular IAs and opens a new avenue of research for developing pharmacological interventions.<\/jats:p>","DOI":"10.1126\/scitranslmed.abq7721","type":"journal-article","created":{"date-parts":[[2023,6,14]],"date-time":"2023-06-14T17:58:28Z","timestamp":1686765508000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":26,"title":["Increased PDGFRB and NF-\u03baB signaling caused by highly prevalent somatic mutations in intracranial aneurysms"],"prefix":"10.1126","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4695-9631","authenticated-orcid":true,"given":"Yasuyuki","family":"Shima","sequence":"first","affiliation":[{"name":"Biomedical Neural Dynamics Collaboration Laboratory, RIKEN Center for Brain Science, Wako, Saitama 351-0198, Japan."},{"name":"Neurodegenerative 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