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The reduction of pericytes is linked to hemorrhage in bAVMs. The Pdgfb\/Pdgfr\u03b2 signaling pathway is crucial for regulating pericyte recruitment during angiogenesis. Here, we show that mice with\n                    <jats:italic>Pdgfr\u03b2<\/jats:italic>\n                    F7 mutations developed cerebrovascular dysplasia in the brain\u2019s angiogenic region, associated with increased pro-angiogenic and inflammatory signaling. Interestingly, the expression of activin receptor-like kinase 1 (Alk1) is decreased in the brain\u2019s angiogenic region of\n                    <jats:italic>Pdgfr\u03b2<\/jats:italic>\n                    F7 heterozygous mice. Overexpression of ALK1 in brain endothelial cells (ECs) reduces angiogenic signaling and the severity of vascular dysplasia in\n                    <jats:italic>Pdgfr\u03b2<\/jats:italic>\n                    F7 heterozygous mice.\n                    <jats:italic>Pdgfr\u03b2<\/jats:italic>\n                    F7 mutations also increased dysplastic vessels and reduced pericyte coverage in the bAVM in endoglin-deficient mice. Endoglin is an AVM causative gene. Our data indicate that\n                    <jats:italic>Pdgfr\u03b2<\/jats:italic>\n                    F7 mutations result in cerebrovascular dysplasia and worsen the bAVM phenotype in endoglin mutant mice by enhancing angiogenesis and inflammation. Overexpression of ALK1 in brain ECs reduces the severity of cerebrovascular dysplasia in\n                    <jats:italic>Pdgfr\u03b2<\/jats:italic>\n                    F7 heterozygous mice through downregulating angiogenic signaling.\n                  <\/jats:p>","DOI":"10.1007\/s10456-026-10044-w","type":"journal-article","created":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T20:57:18Z","timestamp":1777841838000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Platelet-derived growth factor receptor \u03b2 F7 mutations result in and exacerbate the severity of vascular dysplasia in the brain arteriovenous malformation through enhancing angiogenesis"],"prefix":"10.1007","volume":"29","author":[{"given":"Alka","family":"Yadav","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leandro Barbosa","family":"Do Prado","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mustafa","family":"Mohamed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Calvin","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zahra","family":"Shabani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rich","family":"Liang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly","family":"Press","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Courtney","family":"Tom","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ethan A.","family":"Winkler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1566-9877","authenticated-orcid":false,"given":"Hua","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,3]]},"reference":[{"key":"10044_CR1","doi-asserted-by":"publisher","first-page":"349","DOI":"10.1016\/j.wneu.2020.03.109","volume":"138","author":"LF de Rodrigues","year":"2020","unstructured":"de Rodrigues LF, Castro-Afonso LH, Freitas RK, Colli BO, Abud DG (2020) De Novo intracranial arteriovenous malformation-case report and literature review. 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