Targeted S100A8 PP-Cas9@PLGA-apt microparticles reduced cartilage degradation and subchondral bone isomerism in osteoarthritis treatment through JAK/STAT3 pathway modulation.

ABSTRACT: Synovial inflammation caused by osteoarthritis (OA) results in the release of numerous pro-inflammatory factors that promote cartilage degradation and pathological changes of subchondral bone. Nowadays, S100A8 has been recognized as a critical factor in the progression of inflammatory diseases, but its role in OA still needs to be confirmed. At the same time, the gene editing technology has emerged as a novel therapeutic approach for OA, such as clustered regularly interspaced short palindromic repeats (CRISPR/Cas9) technology, but application in inflammatory gene therapy still requires advanced delivery systems to ensure cell-specific targeting and biosafety. In this study, S100A8 was confirmed as a key mediator perpetuating JAK/STAT3 pathway activation in OA progression by integrated RNA

SUBMITTER: Chen Z 

PROVIDER: S-EPMC12528939 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature