{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T19:33:45Z","timestamp":1790883225839,"version":"4.1.0"},"reference-count":76,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2024,1,19]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>\n              Single-nucleotide polymorphisms linked with the rs1474868 T allele (\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              [mitofusin-2] T\/T) in the human mitochondrial fusion protein\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              gene are associated with reduced platelet\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              RNA expression and platelet counts. This study investigates the impact of MFN2 on megakaryocyte and platelet biology.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>\n              Mice with megakaryocyte\/platelet deletion of\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              (\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              [\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              conditional knockout]) were generated using Pf4-Cre crossed with floxed\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              mice. Human megakaryocytes were generated from cord blood and platelets isolated from healthy subjects genotyped for rs1474868. Ex vivo approaches assessed mitochondrial morphology, function, and platelet activation responses. In vivo measurements included endogenous\/transfused platelet life span, tail bleed time, transient middle cerebral artery occlusion, and pulmonary vascular permeability\/hemorrhage following lipopolysaccharide-induced acute lung injury.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Mitochondria was more fragmented in megakaryocytes derived from\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice and from human cord blood with\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              T\/T genotype compared with control megakaryocytes. Human resting platelets of\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              T\/T genotype had reduced MFN2 protein, diminished mitochondrial membrane potential, and an increased rate of phosphatidylserine exposure during ex vivo culture. Platelet counts and platelet life span were reduced in\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice accompanied by an increased rate of phosphatidylserine exposure in resting platelets, especially aged platelets, during ex vivo culture.\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              also decreased platelet mitochondrial membrane potential (basal) and activated mitochondrial oxygen consumption rate, reactive oxygen species generation, calcium flux, platelet-neutrophil aggregate formation, and phosphatidylserine exposure following dual agonist activation. Ultimately,\n              <jats:italic toggle=\"yes\">Mfn2<\/jats:italic>\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice showed prolonged tail bleed times, decreased ischemic stroke infarct size after cerebral ischemia-reperfusion, and exacerbated pulmonary inflammatory hemorrhage following lipopolysaccharide-induced acute lung injury. Analysis of\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              SNPs in the iSPAAR study (Identification of SNPs Predisposing to Altered ALI Risk) identified a significant association between\n              <jats:italic toggle=\"yes\">MFN2<\/jats:italic>\n              and 28-day mortality in patients with acute respiratory distress syndrome.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Mfn2 preserves mitochondrial phenotypes in megakaryocytes and platelets and influences platelet life span, function, and outcomes of stroke and lung injury.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circresaha.123.322914","type":"journal-article","created":{"date-parts":[[2023,12,29]],"date-time":"2023-12-29T05:00:13Z","timestamp":1703826013000},"page":"143-161","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":53,"title":["Mitofusin-2 Regulates Platelet Mitochondria and Function"],"prefix":"10.1161","volume":"134","author":[{"given":"Shancy","family":"Jacob","sequence":"first","affiliation":[{"name":"Molecular Medicine Program, (S.J., Y.K., S. Bhatlekar, F.D., H.B., A.M., V.M., E.T., G.H., N.K., B.K.M., B.J.S., K.H., N.D.T., S. Boudina, R.A.C., M.T.R., P.F.B., A.S.W., J.W.R.), University of Utah, Salt Lake City, UT."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasuhiro","family":"Kosaka","sequence":"additional","affiliation":[{"name":"Molecular Medicine Program, (S.J., Y.K., S. Bhatlekar, F.D., H.B., A.M., V.M., E.T., G.H., N.K., B.K.M., B.J.S., K.H., N.D.T., S. Boudina, R.A.C., M.T.R., P.F.B., A.S.W., J.W.R.), University of Utah, Salt Lake City, UT."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Seema","family":"Bhatlekar","sequence":"additional","affiliation":[{"name":"Molecular Medicine Program, (S.J., Y.K., S. Bhatlekar, F.D., H.B., A.M., V.M., E.T., G.H., N.K., B.K.M., B.J.S., K.H., N.D.T., S. Boudina, R.A.C., M.T.R., P.F.B., A.S.W., J.W.R.), University of Utah, Salt Lake City, UT."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1442-3568","authenticated-orcid":true,"given":"Frederik","family":"Denorme","sequence":"additional","affiliation":[{"name":"Molecular Medicine Program, (S.J., Y.K., S. Bhatlekar, F.D., H.B., A.M., V.M., E.T., G.H., N.K., B.K.M., B.J.S., K.H., N.D.T., S. Boudina, R.A.C., M.T.R., P.F.B., A.S.W., J.W.R.), University of Utah, Salt Lake City, UT."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4994-1269","authenticated-orcid":true,"given":"Haley","family":"Benzon","sequence":"additional","affiliation":[{"name":"Molecular Medicine Program, (S.J., Y.K., S. Bhatlekar, F.D., H.B., A.M., V.M., E.T., G.H., N.K., B.K.M., B.J.S., K.H., N.D.T., S. 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