<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>15(18)</volume><submitter>Tan Y</submitter><pubmed_abstract>&lt;b>Background:&lt;/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. &lt;b>Methods:&lt;/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. &lt;b>Results:&lt;/b> Se@LNT undergoes intracellular metabolic conversion into selenocysteine, which enhances GPX1 activity and promotes redox balance. It exerts triple reg</pubmed_abstract><journal>Theranostics</journal><pagination>9601-9622</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12486268</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease.</pubmed_title><pmcid>PMC12486268</pmcid><pubmed_authors>Zhang F</pubmed_authors><pubmed_authors>Feng L</pubmed_authors><pubmed_authors>Yan Z</pubmed_authors><pubmed_authors>Cao J</pubmed_authors><pubmed_authors>Tan Y</pubmed_authors><pubmed_authors>Gao L</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Xiong W</pubmed_authors><pubmed_authors>Xie B</pubmed_authors></additional><is_claimable>false</is_claimable><name>GPX1-driven selenium nanoplatform reprograms MAMs-mediated organelle crosstalk to reverse inflammatory adipose expansion in thyroid eye disease.</name><description>&lt;b>Background:&lt;/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. &lt;b>Methods:&lt;/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. &lt;b>Results:&lt;/b> Se@LNT undergoes intracellular metabolic conversion into selenocysteine, which enhances GPX1 activity and promotes redox balance. It exerts triple reg</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-07-15T06:52:36.503Z</modification><creation>2026-06-30T03:23:49.791Z</creation></dates><accession>S-EPMC12486268</accession><cross_references><pubmed>41041063</pubmed><doi>10.7150/thno.117582</doi></cross_references></HashMap>