ApoE is a important protein in lipid metabolism, one of those responsible for transporting cholesterols and other lipids around the body. In today’s open access research, the authors present evidence for rising levels of ApoE with aging to degrade the ability of bone to regenerate. This is unfortunate, because it will not be straightforward to just reduce ApoE levels. The protein is vital; a number of serious inherited conditions involve ApoE mutation that leads to greatly increased lipid levels on the bloodstream and organs.
Bone regeneration, and normal tissue maintenance of bone for that matter, is a balance between constant creation and destruction of extracellular matrix structures. Osteoblast cells build bone, and osteoclasts tear it down. Age-related loss of bone density and strength is the result of a growing imbalance that favors osteoclast activity. There is good evidence for numerous mechanisms to be important here, including the usual suspects such as the inflammatory signaling produced by senescent cells. The data here for reversal of loss of regenerative capacity via reduced ApoE levels is quite compelling as an argument for this to be an important proximate mechanism, however.