ArticleArteriosclerosis, thrombosis, and vascular biology2026
Mitochondrial Extracellular Vesicles Enhance Aortic Valve Calcification Via Carnitine O-Octanoyltransferase-Brief Report.
Rei Itagawa, Takehito Okui, Takeshi Tanaka, Yuto Nakamura, Daiki Hosokawa, Cassandra L Clift, Mark C Blaser, Taku Kasai, Luisa Weiss, Mandy E Turner and 4 more
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In one paragraphArticle in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 · Who and what moneyAuthors and funding
14 authors.
Rei ItagawaDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-4343-0321 Takehito OkuiDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0009-0009-2423-8172 Takeshi TanakaDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Yuto NakamuraDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-9608-9553 Daiki HosokawaDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-9117-1387 Cassandra L CliftDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-2441-4251 Mark C BlaserDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-3923-9786 Taku KasaiDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-8075-6099 Luisa WeissDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Mandy E TurnerDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-6431-5077 Marie BillaudDepartment of Medicine, Center for Excellence in Vascular Biology (M.B., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-7591-0362 Masanori AikawaDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-9275-2079 Sasha A SinghDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0003-0929-3164 Elena AikawaDepartment of Medicine, Center for Interdisciplinary Cardiovascular Sciences (R.I., T.O., T.T., Y.N., D.H., C.L.C., M.C.B., T.K., L.W., M.E.T., M.A., S.A.S., E.A.), Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0001-7835-2135 Funding
Improving Mitral Compensation In Ischemic RegurgitationR01HL141917 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI AIKAWA, ELENA, BISCHOFF, JOYCE E. · 2018 to 2021
$5.6MNew driver of fibrosis and calcification in CAVDR01HL147095 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI AIKAWA, ELENA · 2019 to 2022
$2.4MNef in impaired efferocytosis: a novel mechanism for vascular disease in HIVR01HL174066 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Elena Aikawa, Masanori Aikawa · 2024 to 2026
$2.2MPhosphate dysregulation as a driver of age-related vascular diseaseK99HL177272 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI Mandy Elizabeth Mary Turner · 2025 to 2026
$348kDefining Epigenetic Regulation of Translational and Post-Translational Modification Signaling in Aortic Valve Stenosis via Multi-Omics ApproachesK99HL175119 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI CLIFT, CASSANDRA LUCILLE · 2024 to 2025
$229kNHLBI NIH HHS K99 HL175119NHLBI NIH HHS K99 HL177272NHLBI NIH HHS R01 HL141917NHLBI NIH HHS R01 HL147095NHLBI NIH HHS R01 HL174066
6 · The paper itselfAbstract
backgroundCalcific aortic valve disease, commonly manifesting as aortic stenosis, is a leading cause of mortality with no effective therapy. We previously identified CROT (carnitine O-octanoyltransferase) as a mediator of mitochondrial dysfunction and vascular calcification; however, its role in calcific aortic valve disease is unknown. We investigated whether CROT promotes calcific aortic valve disease progression through the release of procalcific mitochondria-derived extracellular vesicles (mitoEVs).
methodsHuman valvular interstitial cells were isolated from aortic valves of patients with aortic stenosis (n=49; n=34 males, n=15 females). Calcification was induced with osteogenic medium and assessed by Alizarin red. Proteomics compared valvular interstitial cells cultured in normal medium or osteogenic medium following scramble or
resultsCROT silencing significantly reduced osteogenic medium-induced calcification in valvular interstitial cells (
conclusionsOsteogenic stress drives mitochondrial fragmentation and procalcific mitoEV release. CROT inhibition restores mitochondrial homeostasis, reduces mitoEV release and calcification, identifying CROT as a potential therapeutic strategy for calcific aortic valve disease.
Indexed as
Aortic ValveAortic Valve StenosisCalcinosisExtracellular VesiclesMitochondriaAgedAnimalsCells, CulturedDisease Models, AnimalFemaleHumansMaleMice, Inbred C57BLMice, KnockoutProteomicsaortic valvecarnitineextracellular vesiclesmitochondriamorbidityproteomics
Identifiers
PMID42093641
PMCPMC13155380
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