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Endoplasmic reticulum (ER) stress and unfolded protein response (UPR) signaling are key mechanisms underlying neovascularization. Mice lacking the UPR regulator Activating Transcription Factor 6 (ATF6) show normal retinal vasculature yet are resistant to pathologic neovascularization, suggesting that ATF6 inhibition may mitigate retinal damage and vision loss from aberrant retinal angiogenesis. We tested Ceapin\u2010A7, a selective ATF6 inhibitor, in\n                    <jats:italic>Vldlr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice, a genetic model of retinal neovascularization. Intravitreal Ceapin\u2010A7 reduced ectopic vascular projections into the outer retina and significantly increased scotopic b\u2010wave amplitude, while a\u2010wave and photopic responses showed no significant difference between groups. Single\u2010nucleus RNA sequencing revealed suppressed ATF6\/UPR gene programs and angiogenic pathways in retinal endothelial cells and reduced M\u00fcller cell gliosis. These findings demonstrate that pharmacologic ATF6 inhibition mitigates retinal neovascularization in\n                    <jats:italic>Vldlr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice and identifies ATF6\/UPR as a therapeutic target for neovascular retinal diseases.\n                  <\/jats:p>","DOI":"10.1096\/fj.202603175r","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T16:01:31Z","timestamp":1790092891000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Ceapin\u2010\n                    <scp>A7<\/scp>\n                    Suppresses\n                    <scp>UPR<\/scp>\n                    Signaling and Mitigates Retinal Neovascularization in\n                    <i>Vldlr<\/i>\n                    <sup>\n                      <i>\u2212\/\u2212<\/i>\n                    <\/sup>\n                    Mice"],"prefix":"10.1096","volume":"40","author":[{"given":"Soyoung","family":"Park","sequence":"first","affiliation":[{"name":"Department of Pathology Stanford University  Stanford California USA"},{"name":"Department of Ophthalmology Stanford University  Stanford California USA"},{"name":"VA Palo Alto Healthcare System  Palo Alto California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angela","family":"Galdamez","sequence":"additional","affiliation":[{"name":"Department of Pathology Stanford University  Stanford California USA"},{"name":"Department of Ophthalmology Stanford University  Stanford California USA"},{"name":"VA Palo Alto Healthcare System  Palo Alto California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Temme","sequence":"additional","affiliation":[{"name":"Department of Pathology Stanford University  Stanford California 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