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In concordance with this regulatory scheme, ablating IGF-IR genes in cultured chondrocytes inhibits the ability of high [Ca 2+ ] e (by 50%) to enhance terminal differentiation and matrix mineralization, supporting a role for IGF-I/IGF-IR signaling in mediating CaSR-induced chondrocyte differentiation (Figure 1)

Clinically applied drugs for the treatment of heart failure are still severely limited by poor delivery efficiency to the heart and off-target consumption

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