Abstract
Improvements in health and nutrition have increased human longevity over the past centuries. Beneficial increases in lifespan, however, are met with novel degenerative and age-related diseases, including atherosclerosis and heart disease, sarcopenia, diabetes, and osteoporosis. The effects of aging upon the skeleton include anatomically heterogeneous involution, alterations in the composition of both the organic and mineral component of the matrix, and accumulation of microdamage. It has been suggested that the process of mechanotransduction within bone is also affected by aging. Within this chapter, we review the process of mechanotransduction in osteogenic cells, highlight those works that have examined age-related changes in mechanotransduction, and discuss mechanosensitive systems implicated in other tissues.
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Notes
- 1.
Interestingly, transgenic mice that lost bone under tail suspension did not require osteocytes to regain bone mass, suggesting that osteocytes are indispensible for bone loss due to unloading, whereas reloading-induced increases in bone mass are osteocyte-independent. These data indicate that, in the absence of osteocytes, osteoblasts are sufficiently mechanosensitive and mechanoresponsive to initiate skeletal adaptation.
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Acknowledgments
This work was supported by NIH NIAMS R03 AR57547 (DCG) and NIH NIAMS R01 AR45989, NIAMS R21 AR45156, and New York Stem Cell Grant N06G-210 (CRJ). The authors are grateful to Dr. C.E. Yellowley for suggestions to Fig. 1, and to Dr. R.Y. Kwon for helpful discussion.
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Genetos, D.C., Jacobs, C.R. (2012). Bone Cell Mechanoresponsiveness. In: Silva, M. (eds) Skeletal Aging and Osteoporosis. Studies in Mechanobiology, Tissue Engineering and Biomaterials, vol 5. Springer, Berlin, Heidelberg. https://doi.org/10.1007/8415_2011_109
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