Several eye diseases exhibit dysregulated immune activity and inflammation as key features due to increased oxidative and altered metabolic stress leading to cell death. There seems to be crosstalk between these components, causing further deposition of immune mediators and cellular debris at the basal layers of the cornea and retina, leading to increased inflammation and neovascularization. The formation of oxidatively modified adducts of proteins and lipids primarily affect their metabolism and clearance from the neuronal cells, causes release of inflammatory cytokines and eventually leads to neurodegeneration. This loss of neurons, in turn induces inflammation and abnormal neovascularization, causing significant loss of vision. Enhanced ROS generation facilitates the formation of protein and lipid adducts that affects gap junctions, solute transfer and autophagy by RPE and macrophages. These conditions are largely treated by providing steroids and anti-VEGF to the patients. However, an effective treatment would be to target these diseases at an early stage in order to avoid the long term use of steroids or repeated doses of steroids and anti-VEGF.
Thus a detailed understanding of these molecular events in disease pathogenesis in the context of oxidative stress, altered metabolic activity, immune activation and inflammation leading to neurodegeneration and/or neovascularization is warranted.
In this Research Topic, we welcome the submission of articles that explore, but are not limited to, the following areas that lead to neurodegeneration and neovascularization:
• Oxidative stress
• Altered metabolic activity
• Immune activation and inflammation
• OMICS based approaches in patients
• In vitro and in vivo models of ocular diseases
• Translational studies
Several eye diseases exhibit dysregulated immune activity and inflammation as key features due to increased oxidative and altered metabolic stress leading to cell death. There seems to be crosstalk between these components, causing further deposition of immune mediators and cellular debris at the basal layers of the cornea and retina, leading to increased inflammation and neovascularization. The formation of oxidatively modified adducts of proteins and lipids primarily affect their metabolism and clearance from the neuronal cells, causes release of inflammatory cytokines and eventually leads to neurodegeneration. This loss of neurons, in turn induces inflammation and abnormal neovascularization, causing significant loss of vision. Enhanced ROS generation facilitates the formation of protein and lipid adducts that affects gap junctions, solute transfer and autophagy by RPE and macrophages. These conditions are largely treated by providing steroids and anti-VEGF to the patients. However, an effective treatment would be to target these diseases at an early stage in order to avoid the long term use of steroids or repeated doses of steroids and anti-VEGF.
Thus a detailed understanding of these molecular events in disease pathogenesis in the context of oxidative stress, altered metabolic activity, immune activation and inflammation leading to neurodegeneration and/or neovascularization is warranted.
In this Research Topic, we welcome the submission of articles that explore, but are not limited to, the following areas that lead to neurodegeneration and neovascularization:
• Oxidative stress
• Altered metabolic activity
• Immune activation and inflammation
• OMICS based approaches in patients
• In vitro and in vivo models of ocular diseases
• Translational studies
