Redox-inflammation pathways in ocular disease: Targets for nutritional modulation

Area of Science:

• Ophthalmology
• Molecular Biology
• Pathology

Background:

• Visual impairment is a significant global health issue stemming from various ocular diseases.
• Oxidative stress and chronic inflammation are common pathogenic factors in anterior and posterior ocular segments.
• Ocular tissues are vulnerable to redox imbalance due to high metabolic demand and light exposure.

Purpose of the Study:

• To review the mechanisms of redox-inflammatory crosstalk in ocular tissues.
• To highlight key molecular pathways involved in ocular disease pathogenesis.
• To discuss the potential of bioactive nutrients in managing these conditions.

Main Methods:

• Literature review focusing on oxidative stress, inflammation, and ocular diseases.
• Analysis of molecular mechanisms including mitochondrial dysfunction, Nrf2-Keap1, NF-κB, MAPK, and PI3K-Akt signaling.
• Examination of tissue-specific responses and the role of nutrients.

Main Results:

• Redox-inflammatory crosstalk, involving pathways like Nrf2-Keap1 and NF-κB, is central to ocular disease progression.
• Specific ocular tissues exhibit distinct disease phenotypes driven by shared molecular mechanisms.
• Bioactive nutrients show therapeutic potential, but clinical outcomes are variable.

Conclusions:

• Shared redox-inflammatory pathways contribute to diverse ocular diseases.
• Targeting these pathways and employing precision nutrition may offer new therapeutic avenues.
• Further mechanism-based clinical trials are needed to optimize treatment strategies.