With advancing age, regulatory pathways involved in bone remodeling are activated inappropriately in smooth muscle cells of blood vessel walls and cardiac tissue. The result is calcification of tissue, making it inflexible, and disrupting the normal elasticity. That leads to hypertension and other, worse cardiovascular issues. Inflammatory signaling and the presence of senescent cells appear to be involved in causing this process, but firmly proven chains of cause and effect are yet to be established, as is the case for all too much of the panoply of dysfunctions that arise in the progression of degenerative aging.
Separately, the mechanisms of bone remodeling are disrupted in bone tissue itself, giving rise to an imbalance between deposition on the part of osteoblast cells and resorption on the part of osteoclast cells. The density and resilience of bone decreases over time, leading to osteoporosis. In today’s review materials, researchers discuss the regulatory mechanisms involved in both osteoporosis and vascular calcification, noting that while incidence of these conditions are correlated with one another to some degree, it remains unclear as to whether one condition is driving the other, or whether they develop
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