Autophagy is the process by which cells break down unwanted biochemicals and damaged components. More autophagy taking place in your cells appears to be all upside based on what we see happening under the hood during calorie restriction, and based on the use of other fairly crude methods of boosting autophagy. It looks very much like increased autophagy increases longevity and improves long term health.
Cellular senescence on the other hand is a mixed bag; a mechanism that does bad things to you so as to avoid worse things. A cell that lapses into a senescent state due to damage no longer divides, but just sits there emitting biochemical signals that harm the immediate cellular environment - and also hopefully flag the cell for destruction by the immune system. On the one hand this is very effective at preventing runaway replication of damaged cells, i.e. cancer. On the other hand, these harmful senescent cells start to accumulate rapidly with advancing age and collectively contribute to the malfunctioning of your tissues and organs.
Nothing in our cellular biochemistry exists in isolation. Our cells are wondrous rats' nests of interconnected mechanisms, feedback loops, dependencies, and other complex evolved machinery. As it turns out, autophagy and cellular senescence are closely linked - which suggests that if we want to cleverly increase autophagy to obtain long-term health benefits akin to those produced by calorie restriction, we can't just run in and pull the first lever we find, otherwise we may find ourselves even more riddled with senescent cells than usual as the years advance. Here's a paper on that subject:
Here we identify autophagy as a new effector mechanism of senescence. ... A subset of autophagy-related genes are up-regulated during senescence: Overexpression of one of those genes, ULK3, induces autophagy and senescence. Furthermore, inhibition of autophagy delays the senescence phenotype, including senescence-associated secretion [of those biochemicals that harm the local cellular environment]. Our data suggest that autophagy, and its consequent protein turnover, mediate the acquisition of the senescence phenotype.
Equally, I'm fairly certain that calorie restricted people are not more riddled with senescent cells than the rest of us, so there has to be a way to usefully enhance autophagy without dragging in undesirable results.
If you want to dig back a way in the Fight Aging! archives, you'll find another mention of a linking point between senescence and autophagy, this time via the noteworthy p53 gene.
Recently it has become clear that p53 not only controls DNA damage responses, senescence and apoptosis but also plays a major role in the control of autophagy. Thus, deletion, depletion, or inhibition of p53 induces autophagy in human, mouse and nematode cells.
p53 has long been seen as controlling an evolutionary trade-off between longevity and cancer resistance: either you boost p53 to get more senescent cells, less cancer, and a shorter life, or you reduce p53 to get more cancer and a longer life. It seems that increased or reduced autophagy might be an important factor in that difference in longevity, setting the issue of cancer to one side. That said, I should mention that particularly clever biological engineering has recently shown that you can selectively boost p53 or introduce telomerase as well so as to have your cake and eat it - obtain less cancer and a longer life.
Young, A., Narita, M., Ferreira, M., Kirschner, K., Sadaie, M., Darot, J., Tavare, S., Arakawa, S., Shimizu, S., Watt, F., & Narita, M. (2009). Autophagy mediates the mitotic senescence transition Genes & Development, 23 (7), 798-803 DOI: 10.1101/gad.519709