{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T06:37:03Z","timestamp":1764571023001,"version":"3.41.2"},"reference-count":66,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,6,30]],"date-time":"2022-06-30T00:00:00Z","timestamp":1656547200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Abdominal aortic aneurysm (AAA) is a life-threatening disease that lacks effective preventive therapies. This study aimed to evaluate the effect of pemafibrate, a selective peroxisome proliferator-activated receptor alpha (PPAR\u03b1) agonist, on AAA formation and rupture.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Experimental AAA was induced by subcutaneous angiotensin II (AngII) infusion in <jats:italic>ApoE<\/jats:italic><jats:sup>\u2013<\/jats:sup><jats:italic><jats:sup>\/<\/jats:sup><\/jats:italic><jats:sup>\u2013<\/jats:sup> mice for 4 weeks. Pemafibrate (0.1 mg\/kg\/day) was administered orally. Dihydroethidium staining was used to evaluate the reactive oxygen species (ROS).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The size of the AngII-induced AAA did not differ between pemafibrate- and vehicle-treated groups. However, a decreased mortality rate due to AAA rupture was observed in pemafibrate-treated mice. Pemafibrate ameliorated AngII-induced ROS and reduced the mRNA expression of interleukin-6 and tumor necrosis factor-\u03b1 in the aortic wall. Gelatin zymography analysis demonstrated significant inhibition of matrix metalloproteinase-2 activity by pemafibrate. AngII-induced ROS production in human vascular smooth muscle cells was inhibited by pre-treatment with pemafibrate and was accompanied by an increase in catalase activity. Small interfering RNA-mediated knockdown of catalase or PPAR\u03b1 significantly attenuated the anti-oxidative effect of pemafibrate.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Pemafibrate prevented AAA rupture in a murine model, concomitant with reduced ROS, inflammation, and extracellular matrix degradation in the aortic wall. The protective effect against AAA rupture was partly mediated by the anti-oxidative effect of catalase induced by pemafibrate in the smooth muscle cells.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fcvm.2022.904215","type":"journal-article","created":{"date-parts":[[2022,6,30]],"date-time":"2022-06-30T07:25:09Z","timestamp":1656573909000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Pemafibrate Prevents Rupture of Angiotensin II-Induced Abdominal Aortic 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