{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T20:48:17Z","timestamp":1790542097411,"version":"4.1.0"},"reference-count":65,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2019,6]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Pathological angiogenesis, such as exuberant retinal neovascularization during proliferative retinopathies, involves endothelial responses to ischemia\/hypoxia and oxidative stress. Autophagy is a clearance system enabling bulk degradation of intracellular components and is implicated in cellular adaptation to stressful conditions. Here, we addressed the role of the ATG5 (autophagy-related protein 5) in endothelial cells in the context of pathological ischemia-related neovascularization in the murine model of retinopathy of prematurity.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              Autophagic vesicles accumulated in neovascular tufts of the retina of retinopathy of prematurity mice. Endothelium-specific\n              <jats:italic>Atg5<\/jats:italic>\n              deletion reduced pathological neovascularization in the retinopathy of prematurity model. In contrast, no alterations in physiological retina vascularization were observed in endothelial-specific ATG5 deficiency, suggesting a specific role of endothelial ATG5 in pathological hypoxia\/reoxygenation\u2013related angiogenesis. Consistently, in an aortic ring angiogenesis assay, endothelial ATG5 deficiency resulted in impaired angiogenesis under hypoxia\/reoxygenation conditions. As compared to ATG5-sufficient endothelial cells, ATG5-deficient cells displayed impaired mitochondrial respiratory activity, diminished production of mitochondrial reactive oxygen species and decreased phosphorylation of the VEGFR2 (vascular endothelial growth factor receptor 2). Consistently, ATG5-deficient endothelial cells displayed decreased oxidative inactivation of PTPs (phospho-tyrosine phosphatases), likely due to the reduced reactive oxygen species levels resulting from ATG5 deficiency.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>Our data suggest that endothelial ATG5 supports mitochondrial function and proangiogenic signaling in endothelial cells in the context of pathological hypoxia\/reoxygenation\u2013related neovascularization. Endothelial ATG5, therefore, represents a potential target for the treatment of pathological neovascularization-associated diseases, such as retinopathies.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.119.309973","type":"journal-article","created":{"date-parts":[[2019,4,18]],"date-time":"2019-04-18T09:02:07Z","timestamp":1555578127000},"page":"1137-1148","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":44,"title":["Endothelial-Specific Deficiency of ATG5 (Autophagy Protein 5) Attenuates Ischemia-Related Angiogenesis"],"prefix":"10.1161","volume":"39","author":[{"given":"David","family":"Sprott","sequence":"first","affiliation":[{"name":"From the Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty (D.S., D.M.P., I.K., A.Z., J.P., A.C., I.M., T.C., A.K.-v.A.), Technische Universit\u00e4t Dresden, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Poitz","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty (D.S., D.M.P., I.K., A.Z., J.P., A.C., I.M., T.C., A.K.-v.A.), Technische Universit\u00e4t Dresden, Germany."},{"name":"Department of Internal Medicine and Cardiology (D.M.P.), Technische Universit\u00e4t Dresden, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irina","family":"Korovina","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty (D.S., D.M.P., I.K., A.Z., J.P., A.C., I.M., T.C., A.K.-v.A.), Technische Universit\u00e4t Dresden, Germany."},{"name":"OncoRay\u2013National Center for Radiation Research in Oncology, Faculty of Medicine (I.K.), Technische Universit\u00e4t Dresden, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Athanasios","family":"Ziogas","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty (D.S., D.M.P., I.K., A.Z., J.P., A.C., I.M., T.C., A.K.-v.A.), Technische Universit\u00e4t Dresden, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Phieler","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty (D.S., D.M.P., I.K., A.Z., J.P., A.C., I.M., T.C., A.K.-v.A.), Technische Universit\u00e4t Dresden, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonios","family":"Chatzigeorgiou","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Chemistry and Laboratory Medicine, Medical Faculty (D.S., D.M.P., I.K., A.Z., J.P., A.C., I.M., T.C., A.K.-v.A.), Technische Universit\u00e4t 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