The p38-activated ER stress-ATF6α axis mediates cellular senescence

What is it about?

While studying the physiological role of the NBR1 molecule, best known as a selective autophagy receptor, we found that NBR1depletion induced cellular senescence. Cellular senescence is thought be a central mechanism for aging and aging-related diseases. It is also known to play an important role in preventing cancer development. This study was conducted to understand the mechanism of cellular senescence induction. Elucidating the mechanism of senescence is important because the knowledge can be utilized to develop drugs or measures to prevent or treat aging-related diseases as well as cancer. We found that ER stress is a crucial cellular event that mediates cellular senescence. It is also identified that ATF6alpha, among the molecules that trigger a cellular response against ER stress, is responsible for senescence induction. In addition, we elucidated participation of other molecules including p38 MAP kinase and NADPH oxidase and how they leaded to ER stress and cellular senescence.

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Why is it important?

Cellular senescence is thought be a central mechanism for aging and aging-related diseases. It is also known to play an important role in preventing cancer development. Therefore, the knowledge on the mechanism of cellular senescence induction can be utilized to develop drugs or measures to prevent or treat aging-related diseases as well as cancer.