Figure 2.

Schematic illustration highlighting the central role of chronic NF-κB activation in inflammation in the elderly and in the development of age-related diseases. Factors known to promote aging phenotypes, such as pro-growth and survival pathways, genotoxic and oxidative stress, DNA damage, telomere shortening and inflammation activate NF-κB. NF-κB in turn acts to promote ageing-related changes by contributing to telomere shortening and positive regulation of the catalytic subunit TERT, cellular senescence, macrophage polarization toward an inflammatory M1 phenotype, proinflammatory secretion of cytokines, mainly TNFα and IL6, and inflammatory responses, which originate a subclinical chronic inflammatory status in aged individuals which can lead to the development of diverse age-associated diseases, including shortening of life-span, progeroid syndromes; eye diseases (glaucoma, DED (dry eye disease etc.), neurodegenerative diseases (AD, Alzheimer’s disease; PD (Parkinson’s disease); ALS (amyotrophic lateral sclerosis) etc.), osteoporosis, osteoarthritis, muscle and heart diseases, atherosclerosis and other disorders such as type 2 diabetes (T2D), obesity and insulin resistant, and hepatic diseases, which have associated an increased risk of developing cancer.