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...
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| Veröffentlicht in: | Cell metabolism Jg. 28; H. 3; S. 337 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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United States
04.09.2018
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| ISSN: | 1932-7420, 1932-7420 |
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| Abstract | 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. |
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| AbstractList | 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.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. 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. |
| Author | Bains, Yasmin Kapahi, Pankaj Gugliucci, Alejandro Chaudhuri, Jyotiska Guha, Sanjib Hall, David Kahn, Arnold Bose, Neelanjan |
| Author_xml | – sequence: 1 givenname: Jyotiska surname: Chaudhuri fullname: Chaudhuri, Jyotiska email: jchaudhuri@buckinstitute.org organization: The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA. Electronic address: jchaudhuri@buckinstitute.org – sequence: 2 givenname: Yasmin surname: Bains fullname: Bains, Yasmin organization: Touro University College of Osteopathic Medicine, Glycation Oxidation and Research laboratory, Vallejo, CA, 94592, USA – sequence: 3 givenname: Sanjib surname: Guha fullname: Guha, Sanjib organization: The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA – sequence: 4 givenname: Arnold surname: Kahn fullname: Kahn, Arnold organization: The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA; University of California, Department of Urology, 400 Parnassus Avenue, San Francisco, CA 94143, USA – sequence: 5 givenname: David surname: Hall fullname: Hall, David organization: The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA – sequence: 6 givenname: Neelanjan surname: Bose fullname: Bose, Neelanjan organization: The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA; University of California, Department of Urology, 400 Parnassus Avenue, San Francisco, CA 94143, USA – sequence: 7 givenname: Alejandro surname: Gugliucci fullname: Gugliucci, Alejandro email: alejandro.gugliucci@tu.edu organization: Touro University College of Osteopathic Medicine, Glycation Oxidation and Research laboratory, Vallejo, CA, 94592, USA. Electronic address: alejandro.gugliucci@tu.edu – sequence: 8 givenname: Pankaj surname: Kapahi fullname: Kapahi, Pankaj email: pkapahi@buckinstitute.org organization: The Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA 94945, USA; University of California, Department of Urology, 400 Parnassus Avenue, San Francisco, CA 94143, USA. Electronic address: pkapahi@buckinstitute.org |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30184484$$D View this record in MEDLINE/PubMed |
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| Title | The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality |
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