Disease models
Several models can efficiently be addressed by our platform. These models will fit with all human medical applications where metabolism dysfunction is involved.
Neurodegenerative diseases
The involvement of oxidative stress in Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), suggest that free radicals play important roles in the onset and progress of neurodegenerative process. The investigation of mitochondrial diseases as a model of neurodegenerative disease, is useful for defining the role of these organelles in normal and pathological conditions.
Atherosclerosis
The oxidative stress as an important trigger in the complex chain of events leading to and promoting atherosclerosis. The expression of chemotactic factors is enhanced by oxidative stress and oxidized LDL. Oxidized LDL, stimulates the release of interleukin-1 from macrophages. The activity of MMPs is also regulated by oxidative stress and appears to be closely linked to smooth muscle cell activation and migration. MMPs have also been implicated in the physiopathology of plaque rupture. Furthermore, ROS can lead to platelet activation and thrombus formation. Therefore, oxidative stress appears to be important in both the early and later stages of the atherosclerotic process.
Diabetes
A chronic elevation of glucose leads to the generation of reactive oxygen species (ROS), resulting in increased oxidative stress in β-cells. As a result, β-cells become worsened with respect to both insulin secretion and action due to their ability to directly damage and oxidize DNA, protein, and lipids. In addition to macromolecular damage, ROS can activate a number of cellular stress-sensitive pathways that have been linked to insulin resistance and decreased insulin secretion. In order to neutralize ROS, cells are equipped with antioxidant defense mechanisms capable of combating oxidative stress. Intriguingly, compared to other tissues, β-cells have a lower abundance of antioxidant defense enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. Thus, due to the low antioxidant defense status of islets, excessive ROS lead to oxidative stress during β-cell dysfunction.