Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction.
A, S., L, M., K, F., B, B., N, H., C, M., J, H., S, E., A, N., & BM, B. (2026). Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1813788
A S, L M, K F, B B, N H, C M, et al. Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction.. Frontiers in immunology. 2026; doi: 10.3389/fimmu.2026.1813788
A S, L M, K F, et al. Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction.[J]. Frontiers in immunology. 2026. DOI: 10.3389/fimmu.2026.1813788.
@article{a2026,
author = {Schlecht A and Müllerbauer L and Fitz K and Brunne B and Hofmann N and Müller C and Hillenkamp J and Ergün S and Neueder A and Braunger BM},
title = {Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction.},
journal = {Frontiers in immunology},
year = {2026},
doi = {10.3389/fimmu.2026.1813788},
note = {PMID: 42433372},
}
TY - JOUR AU - Schlecht A AU - Müllerbauer L AU - Fitz K AU - Brunne B AU - Hofmann N AU - Müller C AU - Hillenkamp J AU - Ergün S AU - Neueder A AU - Braunger BM TI - Endothelial TGFβ signaling modulates choroidal neovascularization severity via myeloid-endothelial cell interaction. T2 - Frontiers in immunology PY - 2026 DO - 10.3389/fimmu.2026.1813788 AN - PMID:42433372 ER -
INTRODUCTION: 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 TGFβ signaling interacts with mononuclear phagocytes (MP), such as microglia to regulate choroidal neovascularization (CNV). METHODS: In this study, we used a laser-induced CNV model in mice with endothelial-specific Tgfbr2 deletion and concomitant MP depletion via PLX5622. RESULTS: We demonstrate that loss of endothelial TGFβ signaling significantly exacerbates CNV. Strikingly, this effect is fully rescued by MP depletion. Transcriptome and RNA localization of CNV lesions identified fibrinogen alpha chain (Fga) as a MP-derived factor that is exclusively upregulated in mice without endothelial TGFβ signaling. DISCUSSION: These findings suggest a novel TGFβ-dependent interaction between endothelial cells and MP that promotes angiogenesis through microglia derived Fga expression.