Figure 1 Main triggers of senescence

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Figure 1 Main triggers of senescence Figure 1 | Main triggers of senescence. Developmental senescence is thought to be induced as part of a physiological programme that depends on p21CIP1, but not on other cyclin-dependent kinase (CDK) inhibitors such as tumour suppressor ARF (p19ARF), p16INK4a or TP53 (Refs 4,5). On the other hand, senescence induced by stress, insults, regeneration, cancer, ageing, diseases and therapy, can vary substantially depending on the stimulus, context or cell type involved. Stress (for example, an insult, cancer, ageing or therapy) usually activates a signalling cascade involving a DNA damage response (DDR) via ATM or ATR kinases, TP53 activation and increased p21Cip1 transcription184,185 and/or induction of p16Ink4a expression via multiple signalling pathways186. Notably, murine oncogene-induced senescence mainly relies on p19ARF, whereas human cells are mainly dependent on p16INK4a signalling38,187. Activation of p21CIP1 and p16INK4a results in inhibition of CDK complexes and retinoblastoma protein (RB) phosphorylation18,19. RAAS, renin–angiotensin–aldosterone system; ROS, reactive oxygen species. Sturmlechner, I. et al. (2016) Cellular senescence in renal ageing and disease Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.183