The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality.
The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality.
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DOI：
10.1016/j.cmet.2018.08.014
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发表时间：
2018-09-04
期刊：
影响因子：
29
通讯作者：
Kapahi P
中科院分区：
文献类型：
--
作者：
Chaudhuri J;Bains Y;Guha S;Kahn A;Hall D;Bose N;Gugliucci A;Kapahi P
晚期糖基化终末产物(AGEs)在核苷酸、脂类和多肽/蛋白质上的积累是包括人类在内的所有真核生物衰老过程中不可避免的组成部分。到目前为止，大量证据表明，年龄及其功能受损的加合物与衰老过程中出现的变化以及许多与年龄相关的疾病的发展有关，并可能是这些变化的原因。然而，关于年龄形成的生物学、这些联系的因果性质以及是否可以制定新的干预措施来预防或减少与年龄有关的损害的负面影响，仍有许多需要了解。为了促进实现这些后一目的，我们展示了如何使用无脊椎动物模型，特别是黑腹果蝇和秀丽线虫，深入探索与年龄相关的途径，并识别和评估将缓解年龄加合物发育的有害影响的药物。Chaudhuri等人。讨论糖酵解副产物导致晚期糖基化终末产物(AGEs)在年龄相关疾病发病中的作用的机制证据。他们概述了模型生物如何揭示这些机制，这些机制将有助于开发更好的疗法来克服糖尿病病理和神经退行性疾病。
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. Chaudhuri et al. discuss mechanistic evidence for the role of glycolytic byproducts that lead to accumulation of Advanced Glycation End products (AGEs) in the onset of age-related diseases. They outline how model organisms can unveil these mechanisms that will help develop better therapeutics to overcome diabetic pathologies and neurodegenerative diseases.
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DOI：
10.1073/pnas.0607260103
发表时间：
2006-10-10
影响因子：
11.1
作者：
Clements, Casey M.;McNally, Richard S.;Ting, Jenny P-Y.
通讯作者：
Ting, Jenny P-Y.
影响因子：
56.9
作者：
BROWNLEE, M;VLASSARA, H;CERAMI, A
通讯作者：
CERAMI, A
DOI：
10.1073/pnas.91.20.9441
发表时间：
1994-09-27
影响因子：
11.1
作者：
BUCALA, R;MAKITA, Z;VLASSARA, H
通讯作者：
VLASSARA, H
影响因子：
8.2
作者：
Brouwers, Olaf;Niessen, Petra M. G.;Schalkwijk, Casper G.
通讯作者：
Schalkwijk, Casper G.
影响因子：
82.9
作者：
Bierhaus, Angelika;Fleming, Thomas;Nawroth, Peter P.
通讯作者：
Nawroth, Peter P.