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Biological Role of Oxidative Stress in Inflammatory Diseases: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 896

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Dear Colleagues,

The imbalance between reactive oxidant species and endogenous antioxidant defense mechanisms promotes the development of a condition of oxidative stress, which has considerable biological consequences. Increasing evidence is proving that oxidative stress plays a pivotal role in the development and progression of inflammation, and thus contributes to the pathophysiology of a number of diseases, such as cancer, cardiovascular diseases, diabetes, and neurodegenerative processes.

Oxidant species influence all phases of the inflammatory response, including the release by damaged tissues of molecules acting as endogenous danger signals. Their sensing by innate immune receptors from the Toll-like (TLRs) and the NOD-like (NLRs) families leads to activation of signaling pathways promoting the adaptive cellular response to such signals.

While we tend to describe oxidative stress simply as harmful for the human body, it is also true that it is exploited as a therapeutic approach to treat clinical conditions such as cancer, with a certain degree of clinical success.

We can conclude that oxidative stress, although being one of the major injuries to individuals’ wellness and health, can also be exploited as a treatment tool.

Therefore, correlations between oxidative stress, inflammation, and disease should be carefully investigated in order to better understand the etiopathogenesis of diseases and to develop ad hoc future treatments.

Dr. Sara Franceschelli
Guest Editor

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Keywords

  • oxidative stress
  • inflammation
  • endogenous antioxidant enzymes

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Published Papers (1 paper)

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Review

20 pages, 2529 KiB  
Review
Role of Oxidative Stress and Inflammation in Age Related Macular Degeneration: Insights into the Retinal Pigment Epithelium (RPE)
by María Elena Ochoa Hernández, Lidianys María Lewis-Luján, María Guadalupe Burboa Zazueta, Teresa Del Castillo Castro, Enrique De La Re Vega, Juan Carlos Gálvez-Ruiz, Sergio Trujillo-López, Marco Antonio López Torres and Simon Bernard Iloki-Assanga
Int. J. Mol. Sci. 2025, 26(8), 3463; https://doi.org/10.3390/ijms26083463 - 8 Apr 2025
Viewed by 394
Abstract
Age-related macular degeneration (AMD) is a leading cause of visual impairment worldwide, characterized by the accumulation of extracellular drusen deposits within the macula. The pathogenesis of AMD is multifactorial, involving oxidative stress, chronic inflammation, immune system dysregulation, and genetic predisposition. A key contributor [...] Read more.
Age-related macular degeneration (AMD) is a leading cause of visual impairment worldwide, characterized by the accumulation of extracellular drusen deposits within the macula. The pathogenesis of AMD is multifactorial, involving oxidative stress, chronic inflammation, immune system dysregulation, and genetic predisposition. A key contributor to disease progression is the excessive accumulation of reactive oxygen species (ROS), which damage retinal pigment epithelium (RPE) cells and disrupt cellular homeostasis. Additionally, immunosenescence and chronic low-grade inflammation exacerbate AMD pathology, further impairing retinal integrity. Despite ongoing research, effective therapeutic options remain limited, and there is no definitive cure for AMD. This review explores the intricate molecular mechanisms underlying AMD, including the role of oxidative stress, chronic inflammation, and genetic factors in RPE dysfunction. Furthermore, we highlight potential therapeutic strategies targeting these pathways, as well as the emerging role of bioinformatics and artificial intelligence in AMD diagnosis and treatment development. By improving our understanding of AMD pathophysiology, we can advance the search for novel therapeutic interventions and preventative strategies. Full article
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