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Age-related alterations—such as downregulation of the WNT (Wingless Integrated Signaling Pathway) and Notch (Neurogenic locus notch homolog) signaling pathways, decreased activity of AMPK (AMP Activated Protein Kinase), PGC-1α (Peroxisome Proliferator Activated Receptor Gamma Coactivator 1a), mTOR (Mechanistic Target of Rapamycin), and WISP1 (WNT1 Inducible Signaling Pathway Protein 1), along with increased levels of TGF-b (Transforming Growth Factor Beta), and miR-34a—contribute to MuSC dysfunction [132,135,136,137,138,139]
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