Advanced glycoxidation end products in chronic diseases-clinical chemistry and genetic background.
Several diseases (atherosclerosis, diabetes mellitus, chronic renal failure) are associated with oxidative and carbonyl stress, microinflammation and eventually autoimmune reaction. Both oxidative and carbonyl stress cause damage to important biological structures-proteins, carbohydrates, lipids and nucleic acids and may enhance inflammatory response. New compounds and modified structures are formed, among them advanced oxidation protein products (AOPP), advanced glycation end products (AGEs-e.g. pentosidine, carboxymethyllysine) and advanced lipoperoxidation end products (ALEs). Accumulation of glycoxidation products, upregulation of protective mechanisms like glyoxalase I as well as enhanced transcription of genes coding for cytokines, growth factors and adhesive molecules via AGE-RAGE (receptor for AGEs) interaction and subsequent increase of classical acute phase reactants (e.g. CRP-C-reactive protein or orosomucoid) can be observed in a variety of chronic diseases. Additionally, several RAGE gene polymorphisms have shown association with some pathological states-diabetic complications, vascular damage, inflammatory response or antioxidant status. Recent advances in understanding the pathogenesis of chronic diseases provide new possibilities for diagnostics and monitoring of severely ill patients, however, further studies are still required to establish efficient therapeutical strategies.
Kalousová
Marta
M
Institute of Clinical Chemistry and Laboratory Diagnostics, First Faculty of Medicine and General University Hospital, Charles University, Katerinská 32, 12108 Prague 2, Czech Republic. marta.kalousova@seznam.cz
Zima
Tomás
T
Tesar
Vladimír
V
Dusilová-Sulková
Sylvie
S
Skrha
Jan
J
D002624:Chemistry, Clinical / Q000379:methods*; D002908:Chronic Disease; D003920:Diabetes Mellitus / Q000235:genetics / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000032:analysis* / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism; D007791:Lactoylglutathione Lyase / Q000235:genetics / Q000378:metabolism; D009711:Nucleotides / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011110:Polymorphism, Genetic; D000067759:Receptor for Advanced Glycation End Products; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D011971:Receptors, Immunologic / Q000235:genetics* / Q000378:metabolism
D017127:Glycation End Products, Advanced; D009711:Nucleotides; D000067759:Receptor for Advanced Glycation End Products; D018160:Receptors, Cytoplasmic and Nuclear; D011971:Receptors, Immunologic; D007791:Lactoylglutathione Lyase