Autophagy and senescence share a number of characteristics, which suggests that 
both responses could serve to collaterally protect the cell from the toxicity of 
external stress such as radiation and chemotherapy and internal forms of stress 
such as telomere shortening and oncogene activation. Studies of oncogene 
activation in normal fibroblasts as well as exposure of tumor cells to 
chemotherapy have indicated that autophagy and senescence are closely related 
but not necessarily interdependent responses; specifically, interference with 
autophagy delays but does not abrogate senescence. The literature relating to 
this topic is inconclusive, with some reports appearing to be consistent with a 
direct relationship between autophagy and senescence and others indicative of an 
inverse relationship. Before this question can be resolved, additional studies 
will be necessary where autophagy is clearly inhibited by genetic silencing and 
where the temporal responses of both autophagy and senescence are monitored, 
preferably in cells that are intrinsically incapable of apoptosis or where 
apoptosis is suppressed. Understanding the nature of this relationship may 
provide needed insights relating to cytoprotective as well as potential 
cytotoxic functions of both autophagy and senescence.