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Special Issue "Redox Biology of Glyoxalases"
A special issue of Antioxidants (ISSN 2076-3921).
Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 44499
Special Issue Editor
Interests: glyoxalases; methylglyoxal; advanced glycation end products; oxidative stress; antioxidants; oncology; toxicology; apoptosis; epithelial-to-mesenchymal transition; epigenetics; epidemiology
Special Issue Information
Glyoxalases, comprising glyoxalase 1 and 2, are enzymes that play a critical role in limiting intracellular accumulation of methylglyoxal (MG), a highly reactive dicarbonyl compound formed as a by-product of different metabolic pathways. MG readily reacts with lipids, nucleic acids, and proteins to form a heterogeneous family of advanced glycation end-products (AGEs). AGEs are able to exert complex pleiotropic effects on normal and pathologic processes in cells, including generation of reactive oxygen species (ROS) and oxidative stress or inflammation, events often culminating in distinct biological outcomes, frequently associated with aging, diabetes, cancer, neurodegenerative, and cardio- and cerebrovascular diseases. However, there is also evidence that some MG-derived AGEs are endowed with antioxidant properties. These apparently divergent functions imply that MG-derived AGEs, and consequently glyoxalases, may exert different or even opposite biological effects within cells, frequently in a context-dependent manner. On the other hand, novel redox-dependent mechanisms are emerging in the complex network of regulation of glyoxalases and MG-derived AGEs.
In this Special Issue, I invite investigators to contribute with original research, perspectives, or review articles that describe the relationship between glyoxalases, MG-derived AGEs, and redox biology as it relates to diverse aspects of applied biology research, such as human biology, health sciences, plant sciences, toxicology, and microbiology. Studies with implications for the development of safe, effective, and innovative preventive and therapeutic strategies, including nutraceutical approaches, to modulate redox-dependent regulation of glyoxalases and/or MG-derived AGEs, and, consequently, cell and tissue dysfunctions, are also welcome.
I hope that this Special issue will provide an instrument for communication and dissemination of the most recent findings about the fascinating and rapidly developing topic, the redox biology of glyoxalases.
I look forward to your contribution.
Prof. Cinzia Antognelli
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- Reactive oxygen/ species
- Advanced glycation end products
- Redox biology
- Redox-dependent cell signaling