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Science Resolves Long-term Dispute of Cell Senescence

Aging or injured cells will enter an aging state, along with the emergence of cell cycle arrest. Cellular senescence is seen by many as the cause of human degradation, and  a variety of geriatric cancer, neurodegenerative diseases and so on. To understand the specific mechanism behind this process, will has important significance in promoting human health. Scientists of Harvard Medical School, Brigham and Women's Hospital and the Howard Hughes Medical Institute has conducted an in-depth study on cell senescence, revealing key control mechanism of this process which solves a long-standing controversy in the field. Related papers published on Science.

It is known that once senescent cells cease growth and proliferation, there will be extensive gene expression changes and a series of pathophysiological processes. For example, the expression levels in senescent cells inflammatory cytokines will be significantly increased, and this phenomenon is called senescence-associated secretory phenotype (SASP). These factors senescent cells secreted will affect the surrounding cells, and inhibition of SASP seem to be able to delay aging. However, people still know little about the regulation of the SASP.

The researchers induced cellular senescence in human fibroblasts, only to find highly expressed genetic element in senescent cells. They found that the transcription factor GATA4 played a key role in the activation of senescence. Under normal circumstances, GATA4 is inhibited by autophagy process.

Autophagy is a highly conserved metabolic process in eukaryotes. Through this process, cells transport the damaged, degenerated, and aging cellular components to lysosomes and digest them. When the cells are aging or damaged, the autophagy will lose control on GATA4, ultimately leading to cell senescence. Studies have shown that the expression of GATA4 SASP can induce the expression of related genes, and and the removal of GATA4 can inhibit the expression of SASP gene.

The role of autophagy in cell senescence has been disputed. Previous studies have found that autophagy is a necessary procedure for cellular senescence, but other studies have indicated that autophagy has a suppressive effect on cell senescence. This study provides a good explanation for these contradictory results : overall autophagy helps build cell senescence, and autophagy for GATA4 inhibit cell senescence. Research indicates, DNA damage response by inhibiting autophagy GATA4 induce inflammation and cell aging.

Journal References:

Serrels et al. Nuclear FAK controls chemokine transcription, Tregs and evasion of anti-tumor immunity. Cell (2015)

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