Ontology highlight
ABSTRACT: Objective
To explore the role and mechanism of transcription factor KLF4 in regulating mitochondrial damage and apoptosis by activating chondrocyte autophagy. Human primary chondrocytes were treated with IL-1β to establish an in vitro osteoarthritis model. KLF4 was overexpressed using lentivirus to intervene in chondrocytes. Cell apoptosis and mitochondrial membrane potential were detected by flow cytometry. Mitochondrial morphology was observed under transmission electron microscopy. Cell ATP level was detected by ELISA. Ca2 + homeostasis was detected by flow cytometry with Fluo-3/AM fluorescence labeling. The expression of autophagy-related proteins Beclin1, P62, and LC3 was detected by WB. The interaction between transcription factor KLF4 and gene p62 promoter was verified by du
SUBMITTER: Feng W
PROVIDER: S-EPMC12480129 | biostudies-literature | 2025 Sep
REPOSITORIES: biostudies-literature