{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T06:10:13Z","timestamp":1792131013974,"version":"4.4.0"},"reference-count":49,"publisher":"Wiley","issue":"23","license":[{"start":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T00:00:00Z","timestamp":1772150400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T00:00:00Z","timestamp":1772150400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Optic neuritis (ON) is a common manifestation of multiple sclerosis (MS), characterized by inflammation and demyelination of the optic nerves. Recent studies indicate increased expression of genes associated with stress granules (SGs) in MS, with T cell intracellular antigen 1 (TIA1) being a key component of SGs. However, the role of TIA1\u2010mediated SGs in MS\u2010ON remains unclear. In experimental autoimmune encephalomyelitis (EAE) mice, a model of MS, TIA1 and G3BP1\n                    <jats:sup>+<\/jats:sup>\n                    (a cell marker of SGs) SGs were upregulated in retinal neurons and optic nerve astrocytes. Knockout of\n                    <jats:italic>Tia1<\/jats:italic>\n                    in the CNS (\n                    <jats:italic>Tia1<\/jats:italic>\n                    <jats:sup>Nestin<\/jats:sup>\n                    \u2010CKO mice) suppressed demyelination, inflammatory infiltration, and retinal ganglion cells (RGCs) loss in EAE mice. Mechanically, RNA\u2010sequencing analysis revealed upregulation of cholesterol synthesis genes such as\n                    <jats:italic>hmgcs1<\/jats:italic>\n                    in\n                    <jats:italic>Tia1<\/jats:italic>\n                    <jats:sup>Nestin<\/jats:sup>\n                    \u2010CKO EAE mice. Furthermore, deletion of\n                    <jats:italic>Tia1<\/jats:italic>\n                    in astrocytes (\n                    <jats:italic>Tia1<\/jats:italic>\n                    <jats:sup>GFAP<\/jats:sup>\n                    \u2010CKO mice) also alleviated demyelination in optic nerves in EAE mice through decreasing SG formation and increasing HMGCS1 expression in Tia1\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    astrocytes by decreasing the sequestration of\n                    <jats:italic>hmgcs1<\/jats:italic>\n                    mRNA into SGs. Treatment with diarylpropionitrile (DPN), an ER\u03b2\u2010ligand, partially restored demyelination in\n                    <jats:italic>Tia1<\/jats:italic>\n                    <jats:sup>GFAP<\/jats:sup>\n                    \u2010CKO EAE mice. These findings uncover the role of TIA1\u2010mediated SG dynamics in MS\u2010ON, highlighting a novel mechanism and potential therapeutic target for treatment.\n                  <\/jats:p>","DOI":"10.1002\/advs.202520299","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T20:57:11Z","timestamp":1773003431000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Astrocytic TIA1\u2010Mediated Stress Granules Promote the Demyelination of Optic Neuritis by Sequestering mRNA of Cholesterol Synthesis Genes in an Experimental Autoimmune Encephalomyelitis Model"],"prefix":"10.1002","volume":"13","author":[{"given":"Zheyu","family":"Fang","sequence":"first","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang China"},{"name":"Department of Neurology The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University  Wenzhou Zhejiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Hua","sequence":"additional","affiliation":[{"name":"Department of Neurology The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang China"},{"name":"Department of Neurology Xuanwu Hospital Capital Medical University National Center for Neurological Disorders  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziwei","family":"Fan","sequence":"additional","affiliation":[{"name":"Department of Orthopedics (Spine Surgery) The First Affiliated Hospital of Wenzhou Medical University  Wenzhou Zhejiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiaxin","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Hepatobiliary and Pancreatic Surgery Department of Surgery School of Medicine Fourth Affiliated Hospital Zhejiang University  Yiwu Zhejiang 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