Redox Status and Bioenergetics Liaison in Cancer and Neurodegeneration
1Department of Biology, University of Rome Tor Vergata, Via della Ricerca Scientifica, 00133 Rome, Italy
2Department of Biochemistry and Molecular Biology, University of Salamanca, Plaza Doctores de la Reina, 37007 Salamanca, Spain
3Department of Genetics, Erasmus Medical Center, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands
Redox Status and Bioenergetics Liaison in Cancer and Neurodegeneration
Description
Cells require a constant supply of energy to sustain fundamental biological processes such as growth, differentiation, and death. In heterotrophic organisms, glycolysis- and mitochondrial-driven oxidation of nutrients to produce ATP and the pentose-phosphate-pathway-dependent generation of NADPH provide, respectively, the energy and the reducing equivalents to cope with endergonic reactions. ATP and NADPH also oversee the control of intracellular redox homeostasis by balancing the generation of reactive oxygen and nitrogen species with their elimination through the synergistic action of antioxidant enzymes and thiol-containing antioxidants (e.g., glutathione and thioredoxin). An increasing body of evidence also reveals how bioenergetics and redox status crosstalk dictates the onset of several pathologies, notably cancer and neurodegenerative diseases.
We invite authors to submit original contributions, in the form of review or original research articles, that will enhance the comprehension of the molecular mechanisms underlying metabolic oxidative stress-relying disorders, support the development of potential new therapies, and further stimulate discussion in this important area of research. We are particularly interested in articles exploring possible converging points between the principal metabolic and redox alterations occurring in neurodegenerative diseases and cancer. Potential topics include, but are not limited to:
- Identifying the implications of redox transduction mechanisms involved in cell response to stressful conditions
- Revisiting the role of different metabolic pathways (e.g., glycolysis versus oxidative phosphorylation) in neuronal and cancer metabolism
- Defining the defects of mitochondrial biogenesis, function, or turnover in physiological alteration underlying neoplastic transformation and neuronal demise
- Characterizing the biochemical transformations of cancer cells and neurons (e.g., glutaminolytic pathway)
- Elucidating the metabolic oxidative stress-dependent activation of apoptosis and autophagy in cancer and neurodegenerative, neuroinflammatory diseases
- Recapitulating the developments in molecular genetics and molecular diagnostics of redox and metabolic markers
Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ijcb/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: