2021 Volume 19 Issue 1 Pages 11-20
Inflammation and pain occur as autoimmune responses to stress acting on the body. The stress-induced autoimmune response, which manifests as microinflammation at its early stage, is a risk factor for aging-related diseases, such as arteriosclerosis. The interaction between oxidative stress and glycative stress affects the human body's immune response. Glycative stress follows two pathways that entail the nonphysiological and post-translational modification of proteins. The first pathway includes an intermediate glycative reaction that involves the reduction of aldehydes, sugars, lipids, and alcohols by carbonylated proteins; the product, i.e., glycation advanced end products (AGEs), binds to RAGE(receptors for AGEs)on macrophages, thus enhancing inflammatory cytokine production. The second pathway alters the mitochondrial TCA cycle and causes the excessive production of fumarate and generation of S-(2-succinyl)cysteine(2SC) by succination of cysteine residues. It is clear that these altered cycles are malignant and worsen inflammation and pain, which further increases glycative stress. Now is the time to find ways to minimize glycative stress. In the future, it is important to learn more about glycative stress and establish and implement appropriate countermeasures.
