The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality

Accumulation of advanced glycation end products (AGEs) on nucleotides, lipids, and peptides/proteins are an inevitable component of the aging process in all eukaryotic organisms, including humans. To date, a substantial body of evidence shows that AGEs and their functionally compromised adducts are...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:Cell metabolism Ročník 28; číslo 3; s. 337
Hlavní autori: Chaudhuri, Jyotiska, Bains, Yasmin, Guha, Sanjib, Kahn, Arnold, Hall, David, Bose, Neelanjan, Gugliucci, Alejandro, Kapahi, Pankaj
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 04.09.2018
Predmet:
Aging - metabolism
Animals
Caenorhabditis elegans - metabolism
Drosophila melanogaster - metabolism
Glycation End Products, Advanced - metabolism
Humans
Metabolic Diseases - metabolism
Mice
Models, Animal
Neurodegenerative Diseases - metabolism
Oxidative Stress
Rats
Signal Transduction
Yeasts - metabolism
ISSN:1932-7420, 1932-7420
On-line prístup:Zistit podrobnosti o prístupe
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Popis
Shrnutí:Accumulation of advanced glycation end products (AGEs) on nucleotides, lipids, and peptides/proteins are an inevitable component of the aging process in all eukaryotic organisms, including humans. To date, a substantial body of evidence shows that AGEs and their functionally compromised adducts are linked to and perhaps responsible for changes seen during aging and for the development of many age-related morbidities. However, much remains to be learned about the biology of AGE formation, causal nature of these associations, and whether new interventions might be developed that will prevent or reduce the negative impact of AGEs-related damage. To facilitate achieving these latter ends, we show how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGE-adduct development.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1932-7420
1932-7420
DOI:10.1016/j.cmet.2018.08.014