{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T19:50:18Z","timestamp":1782157818072,"version":"3.54.5"},"reference-count":45,"publisher":"American Diabetes Association","issue":"7","license":[{"start":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T00:00:00Z","timestamp":1782086400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.diabetesjournals.org\/journals\/pages\/license"}],"funder":[{"DOI":"10.13039\/501100007129","name":"Natural Science Foundation of Shandong Province","doi-asserted-by":"publisher","award":["ZR2020MH174"],"award-info":[{"award-number":["ZR2020MH174"]}],"id":[{"id":"10.13039\/501100007129","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Innovation Project of Jinan Science and Technology Bureau","award":["202333066"],"award-info":[{"award-number":["202333066"]}]}],"content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,7,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Diabetic retinopathy (DR) is a major cause of irreversible vision loss driven primarily by retinal vascular damage, yet its mechanisms remain incompletely understood. Here, we identify calnexin (Canx) as a critical suppressor of pathological angiogenesis in DR. We demonstrate that hyperglycemia synergizes with TNF-\u03b1 to downregulate Canx in mouse retinal microvascular endothelial cells. This loss of Canx activates Nox4, leading to hyperactivation of the Ire1\u03b1\/Xbp1s branch of the unfolded protein response. Consequently, endoplasmic reticulum stress is amplified, pathological Vegfa transcription is upregulated, and the inner blood-retinal barrier is disrupted. In streptozotocin-induced diabetic mouse models, Canx deficiency exacerbated endothelial dysfunction and retinal vascular pathology. Conversely, both adalimumab treatment and adeno-associated virus\u2013mediated Canx overexpression in\u00a0vivo suppressed the Nox4\/Ire1\u03b1\/Xbp1s\/Vegfa cascade, significantly reduced vascular leakage and acellular capillary formation, attenuated retinal thinning, and normalized endothelial cell functions (proliferation, migration, tube formation). Collectively, our findings establish Canx as a key upstream regulator of Vegfa-mediated vascular injury in DR. Our study suggests that targeting Canx, either genetically or via repurposing adalimumab, represents a source-specific strategy to halt DR progression by blocking pathological Vegfa production at its origin.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Article Highlights<\/jats:title>\n                    <jats:p>Diabetic retinopathy (DR) remains a leading cause of blindness, with current interventions often failing to halt progression. In mouse retinal microvascular endothelial cells (mRMVECs), hyperglycemia\/tumor necrosis factor-\u03b1 suppress calnexin (Canx). Canx downregulation drove vascular pathology in mRMVECs via the Nox4\/Ire1\u03b1\/Xbp1s pathway, amplifying endoplasmic reticulum stress and pathological Vegfa production. In streptozotocin-induced diabetic mouse models, Canx overexpression or adalimumab intervention attenuated DR in\u00a0vivo by blocking this cascade. Our findings establish Canx as a critical upstream regulator, proposing Canx-targeted strategies as source-specific therapeutics for DR.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2337\/db25-0756","type":"journal-article","created":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T19:01:56Z","timestamp":1782154916000},"page":"1150-1161","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":0,"title":["The Mechanism of TNF-\u03b1 Combined With High Glucose in Regulating Calnexin Aggravates Endoplasmic Reticulum Stress in Endothelial Cell Injury of Diabetic Retinopathy"],"prefix":"10.2337","volume":"75","author":[{"given":"Yaru","family":"Hou","sequence":"first","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tianran","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaxing","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zirui","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunnan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0290-1545","authenticated-orcid":false,"given":"Yan","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Qilu Hospital of Shandong University, Shandong University , Jinan, Shandong Province, China"},{"name":"School of Medicine, Shandong University , Jinan, Shandong Province, China"},{"name":"NHC Key Laboratory of Otorhinolaryngology, Qilu Hospital of Shandong University , Jinan, Shandong Province, China"},{"name":"Laboratory of Basic Medical Sciences, Qilu Hospital of Shandong University , Jinan, Shandong Province, 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