Recent Advances in Metabolism and Oxidative Stress in Human Diseases 2.0
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".
Deadline for manuscript submissions: 31 May 2025 | Viewed by 241
Special Issue Editors
Interests: bioenergetics; neurosciences; metabolism; photoreceptor
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Cell energy metabolism, the biochemical process responsible for ATP synthesis linked to NAD(P)H turnover, implies the occurrence of oxidative and reductive processes for metabolic energy recruitment and management. Most cell ATP is produced via mitochondrial oxidative phosphorylation (OxPhos), whose efficacy depends on mitochondria networks and ER–mitochondria interactions.
Recent studies have shown that the impairment of structural and functional interactions between ER and mitochondria, in addition to the alteration of the mitochondrial network, affects cell physiology, resulting in the hyperproduction of reactive oxygen species (ROS) and oxidative damage. Although mitochondria represent the center of energy production, they also constitute the principal intracellular sources of ROS. This “double-edged role” configures mitochondria as the organelles in which the energy metabolism encounters redox homeostasis. Indeed, energy metabolism and redox state are inextricably linked in the coordinated regulation of (i) metabolic pathways, (ii) antioxidant systems, (iii) mitochondrial biogenesis and dynamics, and (iv) autophagy and mitophagy. Alterations of the crosstalk between redox homeostasis and cellular metabolism are hallmarks of a wide variety of disease processes. For example, in neurodegenerative disorders like Alzheimer’s and Parkinson’s diseases, oxidative stress has been identified as a key player associated with defects in mitochondrial function, dynamics, and/or degradation. Cardiovascular diseases also exhibit a strong connection with oxidative stress and mitochondrial dysregulation. Metabolic reprogramming of most core metabolic pathways, including those of glucose, glutamine, amino acids, and lipids, as well as increased antioxidant activity, are hallmarks of cancer cells in the various stages of the disease. Moreover, the tumor microenvironment (TME) represents a determinant metabolic barrier that affects T-cell anti-tumor activity. Indeed, the metabolic and nutrient competition in TME implies a metabolic reprogramming of T cells, rendering them dysfunctional and configuring this metabolic switch as a target in order to enhance T-cell-mediated immunity against cancer cells. Notably, recent evidence highlights the connection between ER stress response, oxidative stress, and inflammation in various diseases, emphasizing their roles in immunity and inflammatory/metabolic functions. Understanding the mechanisms and actors involved in the intricate crosstalk between energy metabolism and redox state has the potential to help to identify new therapeutic targets.
This Special Issue, entitled “Recent Advances in Metabolism and Oxidative Stress in Human Diseases 2.0”, invites original research and review articles to contribute to the understanding of the molecular mechanisms that drive metabolic reprogramming, including the metabolic function, biology and redox homeostasis that lead to the development of effective treatments for different diseases.
Prof. Dr. Isabella Panfoli
Dr. Vanessa Cossu
Guest Editors
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Keywords
- antioxidant responses
- redox balance
- ROS
- hematologic oncology
- solid tumors
- immune response
- ATP
- cancer cells
- mitochondria-ER interactions
- endoplasmic reticulum
- glucose metabolism
- inflammation
- mitochondria
- mitochondrial dynamics
- autophagy
- mitophagy
- metabolic plasticity
- metabolism
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