AGEs Contribute to Disc Degeneration via Interaction with RAGE

Advanced glycation endproducts (AGEs) are a form of metabolic waste, sugary compounds that can interact harmfully with structures and cells in the body. A few forms of persistent AGE can form lasting cross-links in the extracellular matrix that change the structural properties of tissues, contributing to the loss of elasticity in skin and blood vessels, for example. Most AGEs are transient compounds, however, associated with the abnormal metabolism of diabetes and the chronic inflammation of aging. Dietary AGEs may also be influential on levels of AGEs in the body, though the size of this contribution is arguable - the body is quite capable of manufacturing significant amounts of AGEs even without a dietary component. Transient AGEs cause chronic inflammation and harmful changes to cell behavior by interacting with the receptor for AGEs (RAGE). In today's open access research paper, researchers show that this contributes meaningfully to the progression of degenerative disc disease, impacting the maintenance of collagen in intervertebral discs. Inhibition of RAGE signaling is thus a potential target for therapies, though finding a way to suppress levels of AGEs - or address causes of rising amounts of AGEs - sounds like a better class of approach. Advanced glycation end products cause RAGE-dependent annulus fibrosus collagen disruption and loss identified using in situ second harmonic generation imaging in mice intervertebral disk in vivo and in organ culture mod...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs