Table 4 Cellular senescence and other age-related mechanisms in “bone-organ” disorders
From: Cellular senescence and other age-related mechanisms in skeletal diseases
Organ | Molecules or signals | Variation | Effect | References |
|---|---|---|---|---|
Skin | Cystatin-A | Down | Inhibits osteogenesis, promotes OCs activation | |
Skeletal muscle | FOXO3 | Down | Inhibits myogenic factors and impairs the maintenance of skeletal homeostasis | |
Nerve | EP4 | Down | Regulates bone homeostasis and promotes regeneration by sensing prostaglandin E2 secreted by OBs | |
Brain | β-amyloid | Up | Elevates OB-derived sclerostin associated with aging increases the production of β-amyloid in the brain and accelerating cognitive impairment | |
Liver | SIRT2 | Up | Downregulates the transfer of LRG1 to bone marrow mononuclear cells, inhibits nuclear translocation of NF-κB p65, activates OCs, and promotes the progression of OP | |
Gut | AMPK-SIRT1 | Down | Increases mitochondrial senescence in BMSCs | |
TWK10 | Down | Increases aging-related bone loss by modulating intestinal dysbiosis and reduces total short-chain fatty acid levels | ||
Microbial tryptophan metabolites | Down | Inhibits osteogenesis and promotes OCs activation by reducing the production of IL-10 by M2 macrophages in the intestinal lamina propria into the bone marrow |
