Advanced Glycation and Lipoxidation End Products
نویسندگان
چکیده
منابع مشابه
Advanced glycation end products
Aging is the progressive accumulation of damage to an organism over time leading to disease and death. Aging research has been very intensive in the last years aiming at characterizing the pathophysiology of aging and finding possibilities to fight age-related diseases. Various theories of aging have been proposed. In the last years advanced glycation end products (AGEs) have received particula...
متن کاملAdvanced glycation end products, soluble receptor for advanced glycation end products, and risk of colorectal cancer.
BACKGROUND Advanced glycation end products (AGE) accumulate in human tissue proteins during aging, particularly under hyperglycemia conditions. AGEs induce oxidative stress and inflammation via the receptor for AGEs (RAGE) and soluble RAGE (sRAGE) can neutralize the effects mediated by RAGE-ligand engagement. METHODS We examined the association between N(ε)-(carboxymethyl)lysine (CML), a prom...
متن کاملProinflammatory effects of advanced lipoxidation end products in monocytes.
OBJECTIVE The reactions of carbohydrate- or lipid-derived intermediates with proteins lead to the formation of Maillard reaction products, which subsequently leads to the formation of advanced glycation/lipoxidation end products (AGE/ALEs). Levels of AGE/ALEs are increased in diseases like diabetes. Unlike AGEs, very little is known about ALE effects in vitro. We hypothesized that ALEs can have...
متن کاملAdvanced glycation end products and diabetic nephropathy.
Chronic hyperglycemia and oxidative stress in diabetes results in the formation and accumulation advanced glycation end products (AGEs). AGEs have a wide range of chemical, cellular, and tissue effects that contribute to the development of microvascular complications. In particular, AGEs appear to have a key role in the diabetic nephropathy. Their importance as downstream mediators of tissue in...
متن کاملAdvanced glycation end products, dementia, and diabetes.
It is becoming abundantly clear that the insight into the pathological process of Alzheimer’s disease (AD) provided through autosomal dominant variants of the condition is only a partial one. The formation and aggregation of Aβ and the phosphorylation and aggregation of tau are clearly part of the core pathogenesis. However, although these may be necessary processes, and indeed in familial form...
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ژورنال
عنوان ژورنال: Journal of the American Society of Nephrology
سال: 2000
ISSN: 1046-6673,1533-3450
DOI: 10.1681/asn.v1191744