Unveiling the Role of Inflammation and Oxidative Stress on Age-Related Cardiovascular Diseases

Figure 5

Many ROS/inflammation interactions are controlled by autoregulatory mechanisms. ROS produced by both NADPH oxidase and mitochondria induce proinflammatory release via NF-κB, such as TNF-α, which modulates an increase in NADPH oxidase and contributes to mitochondrial dysfunction, resulting in more ROS. The upregulation of these mechanisms contributes to cellular damage and eventually drives to cardiovascular diseases.