Figure 7. Autophagy and AMPK play important roles in the regulation of oxidative stress-induced premature senescence in auditory cells.

Hypothesized schematic model. (A) Autophagy impairment leads to the accumulation of lipofuscin and aggregates in cytoplasm, ultimately resulting in auditory cell dysfunction. Our results indicate that premature senescence was induced in our auditory cellular senescence model. (B) The regulation of autophagy through 4EBP1 phosphorylation plays a key role in oxidative stress-induced premature senescence of auditory cells. In addition, autophagy-dependent and independent involvement of AMPK is pivotal for regulating premature senescence in auditory cells.