The emerging evidence suggests that the drawbacks of senescence are twofold. First, one might expect, senescence causes a loss of tissue repair capacity because of cell cycle arrest in progenitor or stem cells. Second, senescent cells produce pro-inflammatory and matrix-degrading molecules (such as IL1-beta, TNF-alpha and MMP, respectively) in what is known as the senescence-associated secretory phenotype (SASP). The SASP is largely initiated by NFkB and p38MAPK signal pathways. I wonder what kind of other signal pathways are involved in SASP? JNK signal, for example, seems to be too transient to cause SASP.
Cell senescence can be both good and bad (i.e. promotes tissue repair or inhibits it) which is likely dependent upon whether senescent cells are removed (i.e. by the immune system) or they persist as may be the case in ageing.
Other pathways regulating the senescent secretome include IL1B, HMGB1, TLR4 and mTOR.
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mTOR signal inhibition with caloric restriction has been shown to contribute to the longer life span, whereas IL-1beta and HMGB1 are reported to be stress signals, which may promote "bad" senescence.
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