chondrocyte redifferentiation by downregulation of the epithelial-tomesenchymal transcription factor Twist-1 and to the selective activation of cell death of senescent cells, decreasing the accumulation of senescent chondrocytes, as detected by the senescent markers p16 and p21, together with decreased expression of SASP components including MMP-3 and IL-6. 3D culture confirmed the restoration of chondrocyte phenotype by showing an increase in the synthesis and deposition of cartilage extracellular matrix components in the presence of both peptides. Conclusions: Our results indicate that peptides from the C-terminal domain of Cx43 efficiently interfere with Cx43 stability and functions promoting redifferentiation and decreasing the accumulation of senescent cells, whose elimination has been lately demonstrated to restore the regenerative capacity of cartilage. We have identified 2 peptides with potential application for the development of new targeted therapy in OA and in other age-related disorders characterized by accumulation of senescent cells and upregulation of Cx43.
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