Fig. 1

Etiology and consequences of cellular senescence contributing to AMD. Cellular senescence is highly relevant to AMD pathogenesis. A variety of factors—telomere dysfunction, oxidative stress, nutrient signals, DNA damage, and inflammatory cytokines—can activate cellular senescence in both mitotic and post-mitotic cells. Senescent cells display altered metabolic function and autophagy activity, as well as a distinctive proinflammatory secretome, which are all interlinked. These processes directly impose a cause-and-effect on one another, further accelerating their progression. The consequences of chronic cellular senescence, such as increased drusen deposition, increased RPE, choriocapillaris and photoreceptor dysfunction and cell loss, and/or neovascularization, ultimately lead to the advanced disease phenotype of macular degeneration