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https://www.selleckchem.com/products/cc-90001.html Lumbar back pain during aging is a major clinical problem, the origins and underlying mechanisms of which are challenging to study. Degenerative changes occur in various parts of the functional spinal unit, such the vertebral endplate and intervertebral disc. The homeostasis of these structural components is regulated by signaling molecules, such as transforming growth factor-β and parathyroid hormone. Previous efforts to understand sources of lumbar back pain focused on sensory innervation in the degenerative intervertebral disc, but intervertebral disc degeneration is frequently asymptomatic. An in vivo mouse model of lumbar spine aging and degeneration, combined with genetic technology, has identified endplate innervation as a major source of lumbar back pain and a potential therapeutic target. In this review, we consider how each structural component of the functional spinal unit contributes to lumbar back pain, how the homeostasis of each component is regulated, and how these findings can be used to develop potential therapies.Aging involves numerous changes in body composition that include a decrease in skeletal muscle mass. The gradual reduction in muscle mass is associated with a simultaneous decrease in muscle strength, which leads to reduced mobility, fragility and loss of independence. This process called sarcopenia is secondary to several factors such as sedentary lifestyle, inadequate nutrition, chronic inflammatory state and neurological alterations. However, the endocrine changes associated with aging seem to be of special importance in the development of sarcopenia. On one hand, advancing age is associated with a decreased secretion of the main hormones that stimulate skeletal muscle mass and function (growth hormone, insulin-like growth factor 1 (IGFI), testosterone and estradiol). On the other hand, the alteration of the IGF-I signaling along with decreased insulin sensitivity also have an importan

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