{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T18:59:17Z","timestamp":1790189957703,"version":"4.1.0"},"reference-count":65,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Myxomatous valve degeneration is a major contributor to adult-onset valvular disease, with congenital valve abnormalities being a predisposing factor. However, the molecular networks that govern heart valve development, particularly postnatal valve maturation, remain poorly understood. This study was designed to investigate the role of GTP\u2011binding SEPTIN proteins in heart valve formation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      We generated endocardial lineage\u2013specific conditional knockout mouse models targeting\n                      <jats:italic toggle=\"yes\">Septin2<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Septin7<\/jats:italic>\n                      , or\n                      <jats:italic toggle=\"yes\">Septin9<\/jats:italic>\n                      . Cardiac phenotypes were assessed using histopathology, immunohistochemistry, and molecular analyses.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Mice lacking\n                      <jats:italic toggle=\"yes\">Septin2<\/jats:italic>\n                      or\n                      <jats:italic toggle=\"yes\">Septin9<\/jats:italic>\n                      developed normally without detectable abnormalities. In contrast,\n                      <jats:italic toggle=\"yes\">Septin7<\/jats:italic>\n                      mutant mice exhibited juvenile lethality due to congestive heart failure caused by severe aortic stenosis. Although valve structure appeared normal at birth,\n                      <jats:italic toggle=\"yes\">Septin7<\/jats:italic>\n                      mutants progressively developed myxomatous degeneration, characterized by leaflet thickening, extracellular matrix disorganization, and inflammatory infiltration. Loss of\n                      <jats:italic toggle=\"yes\">Septin7<\/jats:italic>\n                      disrupted valvular endothelial integrity, with increased intercellular gaps and reduced expression of cell-cell junction proteins. Mechanistically,\n                      <jats:italic toggle=\"yes\">Septin7<\/jats:italic>\n                      ablation inhibited endothelial cell proliferation, most likely through upregulation of the cell cycle inhibitor p21.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Altogether, our findings identify a previously unrecognized role of SEPTIN7 in postnatal heart valve maturation and homeostasis, wherein it safeguards endothelial integrity. This discovery provides critical mechanistic insights into the pathogenesis of pediatric myxomatous valve disease.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.325078","type":"journal-article","created":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T09:00:21Z","timestamp":1787821221000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["SEPTIN7 Deficiency Disrupts Endothelial Integrity and Causes Myxomatous Valve Disease in Juvenile Mice"],"prefix":"10.1161","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5852-4283","authenticated-orcid":true,"given":"Yuan","family":"Fang","sequence":"first","affiliation":[{"name":"The Institute of Cardiovascular Sciences, School of Basic Medical Sciences (Y.F., H.S., J.D., C.Y., S.M., L.Y., X.M., B.L., Y.W.), Xi\u2019an Jiaotong University, China."},{"name":"Cardiovascular Department, The First Affiliated Hospital of Xi\u2019an Jiaotong University, China (Y.F., H.S., J.D., C.Y., S.M., L.Y., X.M., B.L., Y.W.), Xi\u2019an Jiaotong University, China."},{"name":"Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education (Y.F., H.S., J.D., C.Y., S.M., L.Y., X.M., B.L., Y.W.), Xi\u2019an Jiaotong University, China."},{"name":"Cardiometabolic Innovation Center, Ministry of Education (Y.F., H.S., J.D., C.Y., S.M., L.Y., X.M., B.L., Y.W.), Xi\u2019an Jiaotong University, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0288-8579","authenticated-orcid":true,"given":"Hongyu","family":"Su","sequence":"additional","affiliation":[{"name":"The Institute of Cardiovascular Sciences, School of Basic Medical Sciences (Y.F., H.S., J.D., C.Y., S.M., L.Y., X.M., B.L., Y.W.), Xi\u2019an Jiaotong University, China."},{"name":"Cardiovascular Department, The First Affiliated Hospital of Xi\u2019an Jiaotong University, China (Y.F., H.S., J.D., C.Y., S.M., L.Y., X.M., 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