{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T14:51:51Z","timestamp":1791903111166,"version":"4.3.4"},"reference-count":94,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2026,9,15]]},"abstract":"\n BACKGROUND:<\/jats:title>\n \n Atherosclerosis is the primary underlying cause of coronary artery disease.\n LMOD1<\/jats:italic>\n is a coronary artery disease risk gene whose role in coronary artery pathophysiology is unknown. Whole-body loss of\n Lmod1<\/jats:italic>\n causes a lethal neonatal visceral myopathy in mice, necessitating unique approaches for the study of vascular smooth muscle cell (VSMC) phenotypes.\n <\/jats:p>\n <\/jats:sec>\n \n METHODS:<\/jats:title>\n \n Control mice (\n Lmod1<\/jats:italic>\n \n WT<\/jats:italic>\n <\/jats:sup>\n carrying a Cre recombinase allele) and VSMC-restricted\n Lmod1<\/jats:italic>\n knockout mice (\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n ) were subjected to various atherogenic regimens. Atherosclerosis and LMOD1 (leiomodin 1) expression in mouse and human coronary arteries were assessed by histopathology and confocal immunofluorescence microscopy. Coronary arteries from\n Lmod1<\/jats:italic>\n \n WT<\/jats:italic>\n <\/jats:sup>\n and\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice were analyzed with assorted stains and antibodies, immunogold lineage tracing, and spatial metabolomics. Aortic smooth muscle cells from\n Lmod1<\/jats:italic>\n \n WT<\/jats:italic>\n <\/jats:sup>\n and\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice were subjected to lipid loading with or without lentivirus carrying wild-type or actin nucleation\u2013deficient\n Lmod1<\/jats:italic>\n (\n Lmod1<\/jats:italic>\n \n ND<\/jats:italic>\n <\/jats:sup>\n ). Mice harboring an intronic deletion of\n Lmod1<\/jats:italic>\n or\n Lmod1<\/jats:italic>\n \n ND<\/jats:italic>\n <\/jats:sup>\n were engineered using clustered regularly interspaced short palindromic repeats.\n <\/jats:p>\n <\/jats:sec>\n \n RESULTS:<\/jats:title>\n \n A lethal neonatal visceral myopathy occurred in\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice using\n Myh11-CreER<\/jats:italic>\n \n T2<\/jats:italic>\n <\/jats:sup>\n , prohibiting further investigation. In contrast,\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice generated with\n Itga8-CreER<\/jats:italic>\n \n T2<\/jats:italic>\n <\/jats:sup>\n survived and were therefore used in all subsequent studies. Under atherogenic conditions,\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice displayed little vascular disease in several organs but developed diffuse, occlusive coronary atherosclerosis with fibrous caps. No such disease was observed in\n Lmod1<\/jats:italic>\n \n WT<\/jats:italic>\n <\/jats:sup>\n mice. Time-course studies documented lipid insudation and VSMC migration into the intima of coronary arteries of\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice as early as 8 days after the regimen. Immunogold lineage tracing revealed that 46% of coronary plaque cells were of VSMC origin. Spatial metabolomics uncovered multiple lipid species within coronary atheromata of\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice. In vitro studies demonstrated elevated lipid accumulation in\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n VSMCs, which was rescued by viral-mediated\n Lmod1<\/jats:italic>\n \n WT<\/jats:italic>\n <\/jats:sup>\n or\n Lmod1<\/jats:italic>\n \n ND<\/jats:italic>\n <\/jats:sup>\n expression. An intronic deletion of\n Lmod1<\/jats:italic>\n , comprising a conserved orthologous sequence where the single nucleotide variant associated with coronary artery disease exists, showed attenuated LMOD1 expression. Heterozygous\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice, with a comparable reduction in LMOD1, displayed no coronary artery disease. Similarly, VSMC-restricted expression of\n Lmod1<\/jats:italic>\n \n ND<\/jats:italic>\n <\/jats:sup>\n resulted in negligible coronary atherosclerosis.\n <\/jats:p>\n <\/jats:sec>\n \n CONCLUSIONS:<\/jats:title>\n \n Under atherogenic conditions,\n Lmod1<\/jats:italic>\n \n SMKO<\/jats:italic>\n <\/jats:sup>\n mice present with rapid-onset coronary atherosclerosis. LMOD1 safeguards coronary homeostasis, apparently in an actin nucleation\u2013independent manner.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1161\/circulationaha.126.080105","type":"journal-article","created":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T09:00:17Z","timestamp":1785834017000},"page":"992-1011","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":1,"title":["Loss of the Coronary Artery Disease Risk Gene\n LMOD1<\/i>\n in Vascular Smooth Muscle Cells Triggers Rapid-Onset Coronary Atherosclerosis"],"prefix":"10.1161","volume":"154","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8269-1420","authenticated-orcid":true,"given":"Amr R.","family":"Salem","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ajay","family":"Kumar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7169-1166","authenticated-orcid":true,"given":"Jaser","family":"Doja","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alshimaa","family":"Wally","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-3011-1563","authenticated-orcid":true,"given":"Chunyu","family":"Ge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5766-1094","authenticated-orcid":true,"given":"Sabrina","family":"Robichaud","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-5884-5822","authenticated-orcid":true,"given":"Orazio J.","family":"Slivano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1411-153X","authenticated-orcid":true,"given":"Susan H.","family":"Griffin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brendan","family":"Marshall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Perry","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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