Publications by authors named "Birgit Ritschka"

Article Synopsis
  • Young mammals can regenerate certain tissues, but this ability decreases as they mature, possibly due to cellular senescence.
  • In a study of liver regeneration after partial hepatectomy, specific senescence-associated genes (p21, p16, p19) were found to be expressed differently in various cell types as regeneration capacity diminished.
  • Treatment with a drug that inhibits senescence improved liver regeneration by reducing prolonged p21 expression, indicating that targeting cellular senescence may help enhance organ regeneration in young mammals.
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Cellular senescence is a state comprising an essentially irreversible proliferative arrest combined with phenotypic changes and pronounced secretory activity. Although senescence has long been linked with aging, recent studies have uncovered functional roles for senescence in embryonic development, regeneration and reprogramming, and have helped to advance our understanding of this process as a highly coordinated and programmed cellular state. In this Primer article, we summarize some of the key findings in the field and attempt to explain them in a simple model that reconciles the normal and pathological roles for senescence.

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Senescence is a form of cell cycle arrest induced by stress such as DNA damage and oncogenes. However, while arrested, senescent cells secrete a variety of proteins collectively known as the senescence-associated secretory phenotype (SASP), which can reinforce the arrest and induce senescence in a paracrine manner. However, the SASP has also been shown to favor embryonic development, wound healing, and even tumor growth, suggesting more complex physiological roles than currently understood.

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