{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T02:55:14Z","timestamp":1787885714603,"version":"build-2784847793"},"reference-count":80,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      is essential for de novo phopholipogenesis and is impacted by diabetes. We previously demonstrated that conditional knockdown of\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      in the endothelium leads to reduced tissue recovery. Therefore, we hypothesized that\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      overexpression may also be sufficient in promoting postischemic angiogenesis and recovery in the setting of diabetes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      CEPT1 (choline-ethanolamine phosphotransferase 1) content was evaluated in the peripheral arteries of human patients with peripheral artery disease and with or without diabetes. We also engineered a conditional endothelial cell (EC)\u2013specific\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      overexpression mouse (\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">fl\/fl<\/jats:italic>\n                      <\/jats:sup>\n                      <jats:italic toggle=\"yes\">Cre<\/jats:italic>\n                      <jats:sup>+<\/jats:sup>\n                      ) in adult C57BL\/6J (C57 black 6J) mice and performed unilateral hindlimb ischemia to assess the role of\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      in promoting angiogenesis. Murine aortae and ECs were harvested for single-cell RNA sequencing and molecular pathway analysis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      In human arterial intima, CEPT1 was elevated in the setting of peripheral artery disease and diabetes, along with ACOX1 (acyl-coenzyme A oxidase 1), VEGF (vascular endothelial growth factor) R2, p-Akt (phosphorylated Akt), and p-eNOS (phosphorylated endothelial nitric oxide synthase). In mice, single-cell RNA sequencing demonstrated that ECs with\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      overexpression were enriched with wound healing, angiogenesis, sprouting, and cell migration pathways. Diabetic\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">fl\/fl<\/jats:italic>\n                      <\/jats:sup>\n                      <jats:italic toggle=\"yes\">Cre<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic toggle=\"yes\">+<\/jats:italic>\n                      <\/jats:sup>\n                      mice that underwent hindlimb ischemia demonstrated improved hindlimb perfusion and angiogenesis, and their aortic rings had increased ex vivo capillary sprouting.\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      overexpression in ECs significantly increased migration, tubule formation, and proliferation as predicted by single-cell RNA sequencing.\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      overexpression in ECs also led to increased expression of\n                      <jats:italic toggle=\"yes\">Ppar\u03b1<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Acox1<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">Vegfa<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">Vegfr2<\/jats:italic>\n                      . Similarly, treatment with si\n                      <jats:italic toggle=\"yes\">\n                        Ppar\n                        <jats:italic toggle=\"yes\">\u03b1<\/jats:italic>\n                      <\/jats:italic>\n                      and inhibitors for PPAR\u03b1 (peroxisome proliferator-activated receptor \u03b1; GW6471), VEGFR2 (ZM323881), Akt (LY294002), and eNOS (L-NAME [nitro-L-arginine methyl ester]) abrogated CEPT1-induced EC migration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Cept1<\/jats:italic>\n                      overexpression promotes EC function and postischemic recovery. The impact of CEPT1 on ECs is at least in part dependent on p-Akt\/p-eNOS angiogenic signaling and PPAR\u03b1. Because CEPT1 is elevated in diseased human peripheral arterial tissue, these findings suggest that CEPT1 may be playing an important compensatory role in vascular recovery and reperfusion following ischemic injury in the setting of diabetes.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.125.323302","type":"journal-article","created":{"date-parts":[[2025,11,20]],"date-time":"2025-11-20T10:00:19Z","timestamp":1763632819000},"page":"195-209","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["Endothelial CEPT1 Promotes Angiogenesis Through PPAR\u03b1 and VEGF-A Signaling"],"prefix":"10.1161","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8909-8427","authenticated-orcid":true,"given":"Tariq J.","family":"Khan","sequence":"first","affiliation":[{"name":"Division of Vascular Surgery, Department of Surgery (T.J.K., R.M., S.E.-B., L.B., O.S., B.A., M.S.Z., M.A.Z.), 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