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First, the overall gene expression patterns were visualized using principal component analysis (PCA), which revealed evident transcriptomic differences among the PBS, P-Mn@mHSA, and P-Mn/TI@mHSA groups, with no outlier samples detected (Fig
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Importantly, genetic knockdown of RICTOR or pharmacological inhibition of protein kinase B (AKT) (MK-2206) in DMM mouse models restores autophagic flux and alleviates cartilage destruction, highlighting this pathway as a preclinical, but not yet clinically validated, regulator of mitophagy in OA ( In parallel with the canonical PINK1–Parkin pathway, hypoxia-driven receptor-mediated mitophagy pathways, including BNIP3/NIX- and FUN14 domain-containing protein 1 (FUNDC1)-dependent mechanisms, are activated in OA and summarized in Figure 4
