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Cellular senescence: from physiology to pathology
TLDR
In cancer and during active tissue repair, pro-senescent therapies contribute to minimize the damage by limiting proliferation and fibrosis, respectively, and antisenescent therapies may help to eliminate accumulated senescent cells and to recover tissue function.
Tumour biology: Senescence in premalignant tumours
TLDR
It is shown that senescent cells exist in premalignant tumours but not in malignant ones, and that senescence is therefore a defining feature of premalign tumours that could prove valuable in the diagnosis and prognosis of cancer.
Sirt1 protects against high-fat diet-induced metabolic damage
TLDR
Data is presented indicating that beneficial effects of Sirt1 are due to at least two mechanisms: induction of antioxidant proteins MnSOD and Nrf1, possibly via stimulation of PGC1α, and lower activation of proinflammatory cytokines, such as TNFα and IL-6, via down-modulation of NFκB activity.
The Ink4/Arf locus is a barrier for iPS cell reprogramming
TLDR
It is concluded that the silencing of Ink4/Arf locus is rate-limiting for reprogramming, and its transient inhibition may significantly improve the generation of iPS cells.
Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling.
TLDR
The precisely opposite response of normal and immortalized cells to constitutive activation of the MAPK cascade implies that premature senescence acts as a fail-safe mechanism to limit the transforming potential of excessive Ras mitogenic signaling.
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