{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15(18)"],"submitter":["Tan Y"],"pubmed_abstract":["<b>Background:</b> Thyroid eye disease (TED) is a multifactorial autoimmune disorder with limited therapeutic options due to the complexity of its oxidative, metabolic, and inflammatory networks. This study aims to develop a selenium-based nanoplatform that targets mitochondria-ER interactions to reverse inflammatory adipose expansion in TED. <b>Methods:</b> We designed a dual-responsive selenium nanoparticle (Se@LNT) modified with lentinan, capable of ROS/pH-triggered release. Human primary orbital fibroblasts, bioinformatic analysis of public datasets, and TED mouse models were used to investigate the therapeutic mechanism. <b>Results:</b> Se@LNT undergoes intracellular metabolic conversion into selenocysteine, which enhances GPX1 activity and promotes redox balance. It exerts triple reg"],"journal":["Theranostics"],"pagination":["9601-9622"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12486268"],"repository":["biostudies-literature"],"pubmed_title":["GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease."],"pmcid":["PMC12486268"],"pubmed_authors":["Zhang F","Feng L","Yan Z","Cao J","Tan Y","Gao L","Chen X","Xiong W","Xie B"],"additional_accession":[]},"is_claimable":false,"name":"GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease.","description":"<b>Background:</b> Thyroid eye disease (TED) is a multifactorial autoimmune disorder with limited therapeutic options due to the complexity of its oxidative, metabolic, and inflammatory networks. This study aims to develop a selenium-based nanoplatform that targets mitochondria-ER interactions to reverse inflammatory adipose expansion in TED. <b>Methods:</b> We designed a dual-responsive selenium nanoparticle (Se@LNT) modified with lentinan, capable of ROS/pH-triggered release. Human primary orbital fibroblasts, bioinformatic analysis of public datasets, and TED mouse models were used to investigate the therapeutic mechanism. <b>Results:</b> Se@LNT undergoes intracellular metabolic conversion into selenocysteine, which enhances GPX1 activity and promotes redox balance. It exerts triple reg","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-07-15T06:52:36.503Z","creation":"2026-06-30T03:23:49.791Z"},"accession":"S-EPMC12486268","cross_references":{"pubmed":["41041063"],"doi":["10.7150/thno.117582"]}}