<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tang H</submitter><funding>Scientific Fundamental Research Funds of Shandong University</funding><funding>Natural Science Foundation of Shandong Province</funding><funding>National Natural Science Foundation of China</funding><funding>Taishan Scholars</funding><pagination>231</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12754980</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>27(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Temporomandibular joint osteoarthritis (TMJOA) is a prevalent inflammatory disease with unclear pathogenesis. Serum and glucocorticoid-inducible kinase 1 (SGK1) has been implicated in osteoarthritis-related cartilage degeneration. This study investigated the role of SGK1 in a mouse model of TMJOA and explored its mechanism, focusing on SGK1's regulation of Forkhead box O1 (FoxO1) and its subsequent effects on autophagy and extracellular matrix degradation in mouse condylar chondrocytes (MCCs).&lt;h4>Methods&lt;/h4>A TMJOA model was established using unilateral anterior crossbite (UAC), and an SGK1 knockdown model was generated via intra-articular injection of AAV virus.&lt;h4>Results&lt;/h4>SGK1 expression was significantly upregulated in condylar cartilage of UAC-induced TMJOA mice</pubmed_abstract><journal>Arthritis research &amp; therapy</journal><pubmed_title>SGK1 triggers cartilage degradation in TMJOA via FoxO1/autophagy.</pubmed_title><pmcid>PMC12754980</pmcid><funding_grant_id>2019GN091</funding_grant_id><funding_grant_id>ZR2025MS1365</funding_grant_id><funding_grant_id>82201092</funding_grant_id><funding_grant_id>61771290</funding_grant_id><funding_grant_id>tsqn201812137</funding_grant_id><pubmed_authors>Ma C</pubmed_authors><pubmed_authors>Xu M</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Wu G</pubmed_authors><pubmed_authors>Tang H</pubmed_authors><pubmed_authors>Li N</pubmed_authors></additional><is_claimable>false</is_claimable><name>SGK1 triggers cartilage degradation in TMJOA via FoxO1/autophagy.</name><description>&lt;h4>Background&lt;/h4>Temporomandibular joint osteoarthritis (TMJOA) is a prevalent inflammatory disease with unclear pathogenesis. Serum and glucocorticoid-inducible kinase 1 (SGK1) has been implicated in osteoarthritis-related cartilage degeneration. This study investigated the role of SGK1 in a mouse model of TMJOA and explored its mechanism, focusing on SGK1's regulation of Forkhead box O1 (FoxO1) and its subsequent effects on autophagy and extracellular matrix degradation in mouse condylar chondrocytes (MCCs).&lt;h4>Methods&lt;/h4>A TMJOA model was established using unilateral anterior crossbite (UAC), and an SGK1 knockdown model was generated via intra-articular injection of AAV virus.&lt;h4>Results&lt;/h4>SGK1 expression was significantly upregulated in condylar cartilage of UAC-induced TMJOA mice</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-10T04:54:09.316Z</modification><creation>2026-06-10T03:07:19.389Z</creation></dates><accession>S-EPMC12754980</accession><cross_references><pubmed>41470005</pubmed><doi>10.1186/s13075-025-03690-w</doi></cross_references></HashMap>