Special Issue "Glycation and Dicarbonyl Stress in Aging and Disease"
Deadline for manuscript submissions: closed (30 September 2019).
Interests: reactive oxygen species; oxidative stress; redox-responsive pathways; dicarbonyl stress; glycation; methylglyoxal; aging; adaptive response; hormesis; stress response
* h-index: 26
Aging and several age-related diseases share important biochemical and molecular features, in which dicarbonyl stress (DS) and the subsequent glycation process play a key role. DS originates from the increased formation and/or decreased removal of toxic dicarbonyl metabolites, especially methylglyoxal. This, if not counteracted by cellular defense mechanisms, leads to the formation of advanced glycation end-products (AGEs), with consequent cell and tissue dysfunction. Moreover, DS may also derive from exposure to or the intake of exogenous dicarbonyls and AGEs (e.g. through the diet). The accumulation of AGEs has been linked to the activation of pro-inflammatory and pro-oxidant pathways, thus exacerbating the cellular stress. These events are frequently observed in many age-associated pathologies, such as diabetes, cancer, neurodegenerations and cardiovascular diseases. Due to the relevant socio-economic impact, great efforts are currently being undertaken to identify molecular targets able to prevent or limit DS-dependent cell damage.
The aim of this Special Issue is to provide a collection of original and review articles aimed at improving the understanding of the mechanisms underlying the toxicity of AGEs and dicarbonyls in cells and tissues. Studies on innovative strategies, including nutraceutical approaches, to modulate DS-activated intracellular signalling are also welcome.
Prof. Fernanda Amicarelli
Manuscript Submission Information
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- Dicarbonyl stress
- dicarbonyl compounds
- advanced glycation end products (AGEs)
- advanced lipoxidation end products (ALEs)
- oxidative stress
- stress response
- neurodegenerative disease