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Overexpressed ET-1 promoted p16 -positive senescent chondrocytes accumulation and cartilage degradation in TET-1 mice. Selective blockade of ET R, but not ET R, lowered the expression of p16 in ET-1 or H O -induced chondrocyte senescence model, and mitigated the severity of murine PTOA. Intriguingly, reactive oxygen species (ROS) scavenger, Vitamin C, could rescue ET-1-induced chondrocyte senescence in vitro associated with restoration of mitochondrial dynamics. ET-1 could induce chondrocytes senescence and cartilage damages via ET R i

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