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Related Concept Videos

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Related Experiment Video

Updated: May 28, 2026

Quantification of Reactive Oxygen Species Using 2&#8242;,7&#8242;-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in M&#252;ller Glial Cells
14:25

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells

Published on: May 13, 2022

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

P K V Kavyasree1, K Jayadevan2, M Abdullah2

  • 1Departamento de Oftalmología, Government Medical College, Kannur, Kerala, India.

Archivos De La Sociedad Espanola De Oftalmologia
|May 26, 2026
PubMed
Summary

Oxidative stress and inflammation drive vision loss in many eye diseases. Understanding these redox-inflammatory pathways is key to developing new treatments for visual impairment.

Keywords:
Disfunción mitocondrialEnfermedades ocularesEstrés oxidativoInflamaciónInflammationMitochondrial dysfunctionNeurodegeneraciónNeurodegenerationNutrición de precisiónOcular diseasesOxidative stressPrecision nutritionRedox signalingSeñalización redox

Related Experiment Videos

Last Updated: May 28, 2026

Quantification of Reactive Oxygen Species Using 2&#8242;,7&#8242;-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in M&#252;ller Glial Cells
14:25

Quantification of Reactive Oxygen Species Using 2′,7′-Dichlorofluorescein Diacetate Probe and Flow-Cytometry in Müller Glial Cells

Published on: May 13, 2022

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.