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Many patients exhibit poor response or resistance to anti\u2010vascular endothelial growth factor (VEGF) agents. Bruton's tyrosine kinase (BTK) controls the proliferation and function of immune cells. Therefore, we examined the anti\u2010inflammatory and anti\u2010angiogenic effects of BTK inhibition on retinal angiogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>Retinal neovascularisation and vascular leakage in oxygen\u2010induced retinopathy in C57\/BL6J mice were assessed by whole\u2010mount retinal immunofluorescence. PLX5622 was used to deplete microglia and <jats:italic>Rag1<\/jats:italic>\u2010knockout mice were used to test the contribution of lymphocytes to the effects of BTK inhibition. The cytokines, activation markers, inflammatory and immune\u2010regulatory activities of retinal microglia\/macrophages were detected using qRT\u2010PCR and immunofluorescence. NLRP3 was detected by western blotting, and the effects of BTK inhibition on the co\u2010culture of microglia and human retinal microvascular endothelial cells (HRMECs) were examined.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>BTK inhibition suppressed pathological angiogenesis and vascular leakage, and significantly reduced retinal inflammation, which involved microglia\/macrophages but not lymphocytes. BTK inhibition increased anti\u2010inflammatory factors and reduced pro\u2010inflammatory cytokines that resulted from NLRP3 inflammasome activation. BTK inhibition suppressed the inflammatory activity of microglia\/macrophages, and acted synergistically with anti\u2010VEGF without retinal toxicity. Moreover, the supernatant of microglia incubated with BTK\u2010inhibitor reduced the proliferation, tube formation and sprouting of HRMECs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion and Implications<\/jats:title><jats:p>BTK inhibition suppressed retinal neovascularisation and vascular leakage by modulating the inflammatory activity of microglia and macrophages. Our study suggests BTK inhibition as a novel and promising approach for alleviating pathological retinal angiogenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>LINKED ARTICLES<\/jats:title><jats:p>This article is part of a themed issue Drugs and Drug Targets in Metabolic and Chronic Inflammatory Diseases. To view the other articles in this section visit <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v182.20\/issuetoc\">http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v182.20\/issuetoc<\/jats:ext-link><\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.17344","type":"journal-article","created":{"date-parts":[[2024,10,7]],"date-time":"2024-10-07T20:00:57Z","timestamp":1728331257000},"page":"4944-4967","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Bruton's tyrosine kinase inhibition suppresses pathological retinal angiogenesis"],"prefix":"10.1111","volume":"182","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-9234-0689","authenticated-orcid":false,"given":"Siyue","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Ophthalmology Tianjin Medical University General Hospital, Ministry of Education International Joint 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