<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Wu J</submitter><funding>Guangxi Key Laboratory of basic and translational research of Bone and Joint Degenerative Diseases, China</funding><pubmed_abstract>ObjectiveOsteoarthritis (OA) is a prevalent age-related degenerative joint disease characterized by cartilage degeneration, joint pain, and reduced mobility, with aging as the primary risk factor. This study aimed to investigate the role and mechanism of FK506 binding protein 38 (FKBP38) in chondrocyte senescence and OA progression.MethodsFKBP38 expression was detected in articular cartilage from natural aging and OA mouse models. Mice with FKBP38 conditional knockout (FKBP38-cKO) and inducible conditional knockout (FKBP38-iKO) were generated for these models. An adeno-associated virus (AAV) vector overexpressing FKBP38 was injected into wild-type mouse joints. Joint damage was assessed at 8 and 18 months for natural aging or 4 and 8 weeks after DMM surgery by histology.ResultsFKBP38 expre</pubmed_abstract><journal>Cartilage</journal><pagination>19476035251377525</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12497730</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>FKBP38 Alleviates Osteoarthritis Progression by Inhibiting Chondrocyte Senescence.</pubmed_title><pmcid>PMC12497730</pmcid><funding_grant_id>21-220-06</funding_grant_id><pubmed_authors>Liao Z</pubmed_authors><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Zou Z</pubmed_authors><pubmed_authors>Tan X</pubmed_authors><pubmed_authors>Cao H</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Zhou T</pubmed_authors><pubmed_authors>Rao Z</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Li K</pubmed_authors></additional><is_claimable>false</is_claimable><name>FKBP38 Alleviates Osteoarthritis Progression by Inhibiting Chondrocyte Senescence.</name><description>ObjectiveOsteoarthritis (OA) is a prevalent age-related degenerative joint disease characterized by cartilage degeneration, joint pain, and reduced mobility, with aging as the primary risk factor. This study aimed to investigate the role and mechanism of FK506 binding protein 38 (FKBP38) in chondrocyte senescence and OA progression.MethodsFKBP38 expression was detected in articular cartilage from natural aging and OA mouse models. Mice with FKBP38 conditional knockout (FKBP38-cKO) and inducible conditional knockout (FKBP38-iKO) were generated for these models. An adeno-associated virus (AAV) vector overexpressing FKBP38 was injected into wild-type mouse joints. Joint damage was assessed at 8 and 18 months for natural aging or 4 and 8 weeks after DMM surgery by histology.ResultsFKBP38 expre</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Oct</publication><modification>2026-06-05T06:31:20.375Z</modification><creation>2026-06-05T03:06:42.829Z</creation></dates><accession>S-EPMC12497730</accession><cross_references><pubmed>41046448</pubmed><doi>10.1177/19476035251377525</doi></cross_references></HashMap>