{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T16:49:22Z","timestamp":1781801362945,"version":"3.54.5"},"reference-count":41,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2025,7,4]],"date-time":"2025-07-04T00:00:00Z","timestamp":1751587200000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Physiological Reports"],"published-print":{"date-parts":[[2025,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiovascular diseases are the major cause of death worldwide, and their frequency increases with age in association with kidney damage. As a reduction in fusion protein optic atrophy type 1 (Opa1) level in endothelial cells (ECs) decreases the vascular response to flow and increases oxidative stress in perfused kidneys, we hypothesized that reduced Opa1 expression contributes to vascular aging. We used male and female mice with ECs specific Opa1 knock\u2010out (EC\u2010Opa1), and littermate wild\u2010type (EC\u2010WT) mice aged 6 (young) and 20\u2009months (old). Mesenteric resistance arteries (MRA) and kidneys were collected for vascular reactivity and western\u2010blot analysis. In old EC\u2010Opa1 mice, blood urea was greater than in EC\u2010WT mice, and MRA showed reduced endothelium\u2010dependent relaxation. In kidneys, the mitochondria fission protein fission\u20101 (Fis\u20101) and the peroxisome proliferator\u2010activated receptor gamma coactivator\u20101 alpha (Pgc\u20101\u03b1) were increased in old EC\u2010Opa1 mice. The level of caveolin\u20101 expression was greater in old EC\u2010Opa1 mice. Moreover, in kidneys from EC\u2010Opa1 old mice, NADPH\u2010oxidase subunit gp91 expression was greater than in age\u2010matched EC\u2010WT mice. Thus, reduced mitochondrial fusion in mouse ECs altered mesenteric vascular reactivity and increased markers of oxidative stress in aging kidneys. Thus, Opa1 might protect the vascular tree in target organs such as the kidney.<\/jats:p>","DOI":"10.14814\/phy2.70451","type":"journal-article","created":{"date-parts":[[2025,7,5]],"date-time":"2025-07-05T01:50:52Z","timestamp":1751680252000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Altered endothelial mitochondrial Opa1\u2010related fusion in mouse accelerates age\u2010associated vascular and kidney damage"],"prefix":"10.14814","volume":"13","author":[{"given":"Carlotta","family":"Turnaturi","sequence":"first","affiliation":[{"name":"Univ Angers, INSERM, CNRS, MITOVASC Dept, CARME Team, SFR ICAT  Angers France"},{"name":"Department of Pharmacy, School of Medicine and Surgery University of Naples Federico II  Naples Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lo\u00efck","family":"L'Hoste","sequence":"additional","affiliation":[{"name":"Univ Angers, INSERM, CNRS, MITOVASC Dept, 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