{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li L"],"funding":["NHLBI NIH HHS","NINDS NIH HHS","NIH HHS"],"pagination":["2906-2917"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10599232"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["54(11)"],"pubmed_abstract":["<h4>Background</h4>Cerebral cavernous malformations (CCMs) are vascular malformations that frequently cause stroke. CCMs arise due to loss of function in one of the genes that encode the CCM complex, a negative regulator of MEKK3-KLF2/4 signaling in vascular endothelial cells. Gain-of-function mutations in <i>PIK3CA</i> (encoding the enzymatic subunit of the PI3K (phosphoinositide 3-kinase) pathway associated with cell growth) synergize with CCM gene loss-of-function to generate rapidly growing lesions.<h4>Methods</h4>We recently developed a model of CCM formation that closely reproduces key events in human CCM formation through inducible CCM loss-of-function and <i>PIK3CA</i> gain-of-function in mature mice. In the present study, we use this model to test the ability of rapamycin, a clini"],"journal":["Stroke"],"pubmed_title":["mTORC1 Inhibitor Rapamycin Inhibits Growth of Cerebral Cavernous Malformation in Adult Mice."],"pmcid":["PMC10599232"],"funding_grant_id":["R01 NS100949","S10 OD016393","R01 HL094326","P01 NS092521"],"pubmed_authors":["Griffin J","Yang J","Mericko-Ishizuka P","Kahn ML","Alcazar R","Marchuk DA","Ren AA","Li L","Moore T","Burkhardt JK","Awad IA","Shenkar R","Lightle R","Bockman J","Gao S","DeBiasse D","Su YS"],"additional_accession":[]},"is_claimable":false,"name":"mTORC1 Inhibitor Rapamycin Inhibits Growth of Cerebral Cavernous Malformation in Adult Mice.","description":"<h4>Background</h4>Cerebral cavernous malformations (CCMs) are vascular malformations that frequently cause stroke. CCMs arise due to loss of function in one of the genes that encode the CCM complex, a negative regulator of MEKK3-KLF2/4 signaling in vascular endothelial cells. Gain-of-function mutations in <i>PIK3CA</i> (encoding the enzymatic subunit of the PI3K (phosphoinositide 3-kinase) pathway associated with cell growth) synergize with CCM gene loss-of-function to generate rapidly growing lesions.<h4>Methods</h4>We recently developed a model of CCM formation that closely reproduces key events in human CCM formation through inducible CCM loss-of-function and <i>PIK3CA</i> gain-of-function in mature mice. In the present study, we use this model to test the ability of rapamycin, a clini","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Nov","modification":"2026-06-03T07:19:50.978Z","creation":"2025-04-06T09:32:38.732Z"},"accession":"S-EPMC10599232","cross_references":{"pubmed":["37746705"],"doi":["10.1161/strokeaha.123.044108","10.1161/STROKEAHA.123.044108"]}}