Role of Advanced Glycation End Products and Its Receptors in the Pathogenesis of Cigarette Smoke-Induced XXXX .

@entity1095 @entity64 @entity731 @entity3624 @entity5764 @entity26 @entity301 @entity842 @entity453 @entity65
The interaction of advanced glycation end products (AGEs) with its cell-bound receptor @entity5764 increases gene expression and release of proinflammatory cytokines and increase generation of reactive @entity26 species (ROS). Circulating receptors, soluble @entity5764 (sRAGE), and endosecretory @entity5764 (esRAGE) by binding with @entity5764 ligands have protective effects against AGE- @entity5764 interaction. Cigarette smoking is a risk factor for @entity453 , @entity64 , and @entity1095 . This article reviews; if the AGE- @entity5764 axis is involved in the cigarette smoke-induced @entity65 . There are various sources of AGEs in smokers including, gas/tar of cigarette, activation of macrophages and polymorphonuclear leukocytes, uncoupling of endothelial isoform of @entity842 synthase (eNOS) and @entity3624 oxidase. The levels of AGEs are elevated in smokers. Serum levels of sRAGE have been reported to be reduced, elevated, or unchanged in smokers. Mostly the levels are reduced. There is one article which shows an elevation of levels of sRAGE in smokers. Serum levels of esRAGE are unaltered in smokers. Mechanism of AGE- @entity5764 -induced @entity731 has been discussed. @entity731 leads to the @entity65 . It has been suggested that ratio of AGE/sRAGE or AGE/esRAGE is useful in determining the deleterious effects of AGE- @entity5764 interaction in smokers. sRAGE alone is not a good marker for smoke-induced @entity65 . In conclusion cigarette smoke induces formation of AGEs and reduces sRAGE resulting in the development of @entity731 and related @entity301 , @entity64 , and @entity1095 . Ratio of AGEs/sRAGE is a better marker for @entity65 than AGEs or sRAGE alone in smokers.
