Abstract
The present study aimed to examine the impact of mitochondrial sirtuin 3 (SIRT3) on the degenerative rotator cuff injury, which is a prevalent issue among the elderly population primarily due to aging-related tissue degradation. The study hypothesized that SIRT3, as a major deacetylase in mitochondria, is a significant factor in controlling the quality of mitochondria and the deterioration of fibrocartilage, a crucial component of the rotator cuff. Results showed that the aging process led to weakened biomechanical properties and degeneration of the fibrocartilage layer in mice, accompanied by a decrease in SIRT3 expression. SIRT3 activation ameliorated the aging-related disruption of chondrocyte phenotype and fibrocartilage degradation. SIRT3 activator honokiol improved the phenotype of senescent chondrocytes and promoted rotator cuff healing in aged mice through SIRT3 activation. In conclusion, the findings suggested that the decline in SIRT3 levels with age contributes to rotator cuff degeneration and chondrocyte senescence, and that SIRT3 activation through the use of honokiol is an effective approach for promoting rotator cuff healing in the elderly population.
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