{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,30]],"date-time":"2026-08-30T20:29:35Z","timestamp":1788121775514,"version":"build-2803163510"},"reference-count":36,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T00:00:00Z","timestamp":1754956800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T00:00:00Z","timestamp":1754956800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Developmental Neurobiology"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Diabetic retinopathy (DR), a prevailing manifestation among diabetic patients, occurs as a major sight\u2010threatening disorder.\n                    <jats:italic>Dectin\u20101<\/jats:italic>\n                    , as an innate immune receptor, has been notified as a critical modulator of diabetes mellitus. In this context, the implication of\n                    <jats:italic>Dectin\u20101<\/jats:italic>\n                    in the process of DR that is still a conundrum will be addressed here. The diabetic mouse model was established by intraperitoneal injection of streptozotocin (STZ), and human microglia cells (HMC3) were subjected to high glucose (HG) to create cellular models of diabetes. Glucose level and body weight were recorded in mice. Reverse transcription\u2010quantitative PCR (RT\u2010qPCR) and western blotting checked\n                    <jats:italic>Dectin\u20101<\/jats:italic>\n                    expression. RT\u2010qPCR, enzyme\u2010linked immunosorbent assay (ELISA), and western blotting appraised the inflammatory levels. Immunofluorescence staining and western blotting ascertained the expression of IBA\u20101 and tight junction proteins. Besides, western blotting also examined albumin expression. Terminal\u2010deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assay and western blotting assayed the apoptotic level.\n                    <jats:italic>Dectin\u20101<\/jats:italic>\n                    was highly expressed in both retinal tissues of diabetic mice and HG\u2010exposed HMC3 cells.\n                    <jats:italic>Dectin\u20101<\/jats:italic>\n                    antagonist laminarin (LAM) observably repressed microglia activation, inflammatory reaction, and blood\u2013retinal barrier (BRB) leakage both in vitro and in vivo. Moreover, LAM produced anti\u2010apoptotic effect in vivo. To sum up,\n                    <jats:italic>Dectin\u20101<\/jats:italic>\n                    inhibitor might block the inflammatory cascade and protect against BRB disruption in DR.\n                  <\/jats:p>","DOI":"10.1002\/dneu.22997","type":"journal-article","created":{"date-parts":[[2025,8,12]],"date-time":"2025-08-12T07:10:48Z","timestamp":1754982648000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["<i>Dectin\u20101<\/i>\n                    Drives Diabetic Retinopathy via Inducing Microglia\u2010Mediated Inflammation and Blood\u2013Retinal Barrier Breakdown"],"prefix":"10.1002","volume":"85","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-7360-7635","authenticated-orcid":false,"given":"Lei","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Ophthalmology The First Affiliated Hospital of Anhui Medical University  Hefei Anhui China"},{"name":"Department of Ophthalmology Fuyang 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