Oxidative Stress, Mitochondrial Dysfunction, and Redox Signaling in Disease
This community investigates how reactive oxygen species and mitochondrial function regulate cell survival, death, and inflammation, with a focus on understanding and treating conditions like cancer, neurodegeneration, and metabolic disorders.
The work centers on the mechanisms of oxidative stress and the antioxidant responses that counteract it. Recurring themes include the role of reactive oxygen species in signaling pathways, the impact of mitochondrial dysfunction on cellular health, and the regulation of cell death processes such as apoptosis and ferroptosis. Researchers frequently examine these dynamics in the context of specific diseases, including breast and lung cancer, Alzheimer’s disease, and type 2 diabetes. Common experimental models involve human cell lines, mice, and rats, with a strong emphasis on in vitro assays and in vivo interventions. The literature also highlights the interplay between inflammation, specifically the NLRP3 inflammasome, and redox balance, as well as the therapeutic potential of targeting these pathways with antioxidants or other modulators.
The largest share of this research is found in oxygen studies, accounting for 5.4% of all tracked oxygen research, and 29,869 papers here. Hydrogen and bromine research also contribute significantly, with shares of 1.0% and 3.0% respectively.
This community comprises 78,946 papers, publishing most frequently in the Journal of Biological Chemistry, Antioxidants, and Free Radical Biology and Medicine. Recent work continues to explore the therapeutic implications of reactive oxygen species in cancer and the role of neuroinflammation in neurodegenerative diseases, as well as the assessment of antioxidant activity in various biological contexts.