{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T04:50:58Z","timestamp":1782449458633,"version":"3.54.5"},"reference-count":92,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T00:00:00Z","timestamp":1782432000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>The blood-retinal barrier (BRB) is essential for maintaining retinal homeostasis, consequently its disruption contributes to pathological angiogenesis in diseases such as neovascular age-related macular degeneration (nAMD). Choroidal neovascularization (CNV) is considered as a hallmark of nAMD. These newly formed vessels break through the BRB leading to rapid and severe vision loss. Here, we investigated how endothelial TGF\u03b2 signaling interacts with mononuclear phagocytes (MP), such as microglia to regulate choroidal neovascularization (CNV).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this study, we used a laser-induced CNV model in mice with endothelial-specific Tgfbr2 deletion and concomitant MP depletion via PLX5622.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We demonstrate that loss of endothelial TGF\u03b2 signaling significantly exacerbates CNV. Strikingly, this effect is fully rescued by MP depletion. Transcriptome and RNA localization of CNV lesions identified fibrinogen alpha chain (\n                      <jats:italic>Fga<\/jats:italic>\n                      ) as a MP-derived factor that is exclusively upregulated in mice without endothelial TGF\u03b2 signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      These findings suggest a novel TGF\u03b2-dependent interaction between endothelial cells and MP that promotes angiogenesis through microglia derived\n                      <jats:italic>Fga<\/jats:italic>\n                      expression.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1813788","type":"journal-article","created":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T04:35:32Z","timestamp":1782448532000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Endothelial TGF\u03b2 signaling modulates choroidal neovascularization severity via myeloid\u2013endothelial cell interaction"],"prefix":"10.3389","volume":"17","author":[{"given":"Anja","family":"Schlecht","sequence":"first","affiliation":[{"name":"Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf","place":["Hamburg, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisa","family":"M\u00fcllerbauer","sequence":"additional","affiliation":[{"name":"Institute of Anatomy and Cell Biology, Julius-Maximilians-University Wuerzburg","place":["Wuerzburg, 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