Switching off ALPL gene contributes to bone aging
In a recent open-access study, published in Bone Research by scientists at the Xi’an Institute of Tissue Engineering and Regenerative Medicine, they describe how the ALPL gene influences bone aging and suggest that metformin could be a viable option as a therapeutic to prevent it.
Study Abstract
Hypophosphatasia and early onset bone dysplasia are caused by mutations in the alkaline phosphatase gene (Alpl), which is found in the bones, kidneys, liver and liver. This suggests that this gene plays a major role in bone development. However, it is not known how and where Alpl affects bone ageing. We found that ablation of Alpl induced prototypical premature ageing features, such as bone mass loss, marrow fat accumulation, and elevated expression of p16INK4A(p16) and p53, due to senescence, and impaired differentiation, in mesenchymal cells (MSCs). Alpl-deficiency in MSCs increases ATP release, and decreases ATP hydrolysis. The excess extracellular ATP, then, is internalized by MSCs, causing an increase in intracellular ATP. This, in turn causes a switch in cell fate of MSCs.
Source:
https://www.leafscience.org/switching-off-alpl-gene-contributes-to-bone-aging/
