Special Issue "Cellular Redox Mechanisms in Inflammation and Programmed Cell Death"
Deadline for manuscript submissions: 1 March 2024 | Viewed by 1012
Redox reactions play an important role in the regulation of physiological processes. Cellular redox balance can vary widely dependently on cell activity and homeostatic capacity, as well as exposure to stress factors. Normally, redox reactions are strictly controlled; however, during inflammation and programmed cell death (e.g., apoptosis and ferroptosis), increased oxidant production and redox dysregulation contribute to cell injury, culminating in cell demise. Even in these extreme conditions, there are regulatory factors that control the poorly balanced redox processes and limit the spreading of cell death and tissue damage. Notably, inflammatory responses and cell death programs include three stages: initiation, progression, and termination (or cell removal). At all stages, reactive oxygen species and redox enzymes are the key players in the regulation of physiological processes.
The research topics of this Special Issue on redox mechanisms involved in the regulation of inflammation and programmed forms of cell death include the following:
- The radical-generating activity of neutrophils and macrophages in the initiation stage of inflammation.
- The enzymatically controlled production and dismutation of redox-active molecules: NADPH-oxidase (and other Nox), myeloperoxidase, superoxide dismutases, etc.
- The iron-dependent oxidation of cellular lipids and the synthesis of lipid mediators.
- NO• as a regulator of inflammation and cell death.
- Enzymatic and non-enzymatic antioxidants that contribute to the suppression of oxidative stress (thioredoxin family proteins, glutathione peroxidases/reductases, etc.)
- Redox signaling aimed at the removal of dead and damaged cells, and phagocyte redox-activity.
We welcome the submission of research reports, reviews, and mini-reviews that are within the scope of these subjects.
Dr. Irina I. Vlasova
Manuscript Submission Information
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- reactive oxygen species
- nitric oxide
- redox-active enzymes
- lipid oxidation
- inflammatory response