Oxidative Stress in Human Diseases
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: 30 June 2025 | Viewed by 154
Special Issue Editor
Interests: oxidative stress; diabetes; natural antioxidants; asthma; free radicals
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Increasing scientific evidence confirms that the combination of reactive oxygen species (ROS) overproduction, oxidative stress (OS), and hyperinflammation can cause endothelial layer damage, which eventually leads to endothelial dysfunction. Oxidative stress occurs due to the imbalance between the production of ROS and the availability of antioxidants or radical scavengers. The excess ROS produced can either oxidize biomolecules or structurally modify lipids, proteins, and genes to trigger signaling cascades, leading to the onset and progression of inflammatory diseases. Inflammation causes immune cells to secrete various cytokines and chemokines to recruit other immune cells to the site of oxidative stress/infection. Reflexively, enhanced ROS generation by immune cells at the site of inflammation causes oxidative stress and tissue injury. The inflammatory-initiated endothelial dysfunction can promote chronic inflammation, thrombosis, atherosclerosis, and lung injury. The generation of a large amount of mitochondrial reactive oxygen species (mtROS) and their excess causes OS, which can promote inflammation and cause chronic endothelial dysfunction.
Dr. Galina Nikolova
Guest Editor
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Keywords
- inflammation
- oxidative stress
- free radicals
- proteins
- lipids
- DNA damage
- biomarkers
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