Résumé
Purpose (the aim of the study): Osteoarthritis (OA) is a leading cause of joint dysfunction, with aging being a primary risk factor. Naturally aged mice develop OA-like features, including cartilage defects, meniscal calcifications and fibrosis. However, little is known about how the synovial tissue reacts upon natural aging and the underlying cellular and moleculardrivers of these changes are not fully elucidated. This study aims to map the synovial tissue microenvironment in aged mice at single-cell resolution to uncover age-associated cellular deficits and their contribution to joint fibrosis.