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doi: 10.1161/CIRCULATIONAHA.117.027575

At the same time, these mediators drive heightened mitochondrial respiration in chondrocytes, generating excess reactive oxygen species (ROS) that damage mitochondria and promote chondrocyte apoptosis and autophagy (Vonk et al., 2018

Furthermore, we identified the underlying molecular mechanisms: Wnt induction of IGF1 depends on -catenin and subsequent binding of Wnt transcription factor TCF4 to the IGF1 gene promoter