Fig. 8: Hypothetical model of P53 and Parkin co-regulating mitophagy in BMSCs to interfere with cell stress-induced apoptosis and senescence. | Cell Death & Disease

Fig. 8: Hypothetical model of P53 and Parkin co-regulating mitophagy in BMSCs to interfere with cell stress-induced apoptosis and senescence.

From: P53 and Parkin co-regulate mitophagy in bone marrow mesenchymal stem cells to promote the repair of early steroid-induced osteonecrosis of the femoral head

Fig. 8

Under OS, mitochondrial function is impaired and damaged mitochondria release excessive ROS, which can further damage the mitochondria, creating a vicious circle. Moreover, ROS can upregulate P53 expression via the DDR and mTOR pathways. P53 binds to Parkin and inhibits its mitochondrial translocation, the ubiquitination of mitochondrial outer-membrane proteins was inhibited. Eventually, the level of mitophagy decreased, and a large number of mitochondria accumulated in the cells, resulting in apoptosis and senescence of the cells. DDR = DNA damage response; mTOR = mammalian target of rapamycin.

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