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

Figure 6

The crosstalk between Nrf-2 and NF-κB transcription factors. The stress environment caused by oxidative stress leads to functional modifications in both Nrf-2 and NF-κB transcription factors. Oxidation occurs at the thiol’s sites of cysteine residues, allowing dissociation with their cytosolic inhibitors (Keap1 and IκB, respectively), leading to nucleus translocation and consequent encoding of target genes. Oxidative stress can interfere in both pathways indirectly by activating signalling pathways, such as ERK1/2, MAPK, JNK, and p38, which leads to the phosphorylation of these transcription factors. However, in basal situations, Nrf-2 and NF-κB are degraded via proteasome, which maintain homeostasis.