Advanced glycoxidation end products in chronic diseases-clinical chemistry and genetic background
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
16084533
DOI
10.1016/j.mrfmmm.2005.03.024
PII: S0027-5107(05)00268-X
Knihovny.cz E-resources
- MeSH
- Chronic Disease * MeSH
- Kidney Failure, Chronic complications metabolism MeSH
- Diabetes Mellitus genetics metabolism MeSH
- Chemistry, Clinical methods MeSH
- Lactoylglutathione Lyase genetics metabolism MeSH
- Humans MeSH
- Nucleotides metabolism MeSH
- Oxidation-Reduction MeSH
- Oxidative Stress MeSH
- Polymorphism, Genetic MeSH
- Glycation End Products, Advanced analysis metabolism MeSH
- Receptor for Advanced Glycation End Products MeSH
- Receptors, Cytoplasmic and Nuclear metabolism MeSH
- Receptors, Immunologic genetics metabolism MeSH
- Inflammation etiology metabolism MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Lactoylglutathione Lyase MeSH
- Nucleotides MeSH
- Glycation End Products, Advanced MeSH
- Receptor for Advanced Glycation End Products MeSH
- Receptors, Cytoplasmic and Nuclear MeSH
- Receptors, Immunologic MeSH
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.
References provided by Crossref.org
