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Fenofibrate, a PPAR\u03b1 agonist and lipid-lowering agent, decreases amputation incidence in patients with diabetes. Because we previously observed that CEPT1 is elevated in carotid plaque of patients with diabetes, we evaluated the role of CEPT1 in peripheral arteries and PPAR\u03b1 phosphorylation (Ser12). CEPT1 was found to be elevated in diseased lower-extremity arterial intima of individuals with peripheral arterial disease and diabetes. To evaluate the role of Cept1 in the endothelium, we engineered a conditional endothelial cell (EC)\u2013specific deletion of Cept1 via induced VE-cadherin-CreERT2\u2013mediated recombination (Cept1Lp\/LpCre+). Cept1Lp\/LpCre+ ECs demonstrated decreased proliferation, migration, and tubule formation, and Cept1Lp\/LpCre+ mice had reduced perfusion and angiogenesis in ischemic hind limbs. Peripheral ischemic recovery and PPAR\u03b1 signaling were further compromised by streptozotocin-induced diabetes and ameliorated by feeding fenofibrate. Cept1 endoribonuclease-prepared siRNA decreased PPAR\u03b1 phosphorylation in ECs, which was rescued with fenofibrate but not PC16:0\/18:1. Unlike Cept1Lp\/LpCre+ mice, Cept1Lp\/LpCre+Ppara\u2212\/\u2212 mice did not demonstrate hind-paw perfusion recovery after feeding fenofibrate. Therefore, we demonstrate that CEPT1 is essential for EC function and tissue recovery after ischemia and that fenofibrate rescues CEPT1-mediated activation of PPAR\u03b1.<\/jats:p>","DOI":"10.2337\/db20-0635","type":"journal-article","created":{"date-parts":[[2020,11,19]],"date-time":"2020-11-19T17:52:18Z","timestamp":1605808338000},"page":"549-561","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":19,"title":["CEPT1-Mediated Phospholipogenesis Regulates Endothelial Cell Function and Ischemia-Induced Angiogenesis Through PPAR\u03b1"],"prefix":"10.2337","volume":"70","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6443-4527","authenticated-orcid":false,"given":"Mohamed A.","family":"Zayed","sequence":"first","affiliation":[{"name":"Section of Vascular Surgery, Department of Surgery, Washington University School of Medicine in St. Louis, St. Louis, MO"},{"name":"Division of Molecular Cell Biology, Washington University 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