An appreciation of reliability theory is a good way to better put into context ongoing research into the cellular and molecular mechanics of aging. Reliability theory was developed to better predict the failure rates and times to failure of complex systems consisting of many redundant components - such as ships, electronic circuitry, or even we humans:
The failure of mechanical devices such as ships, trains, and cars, is similar in many ways to the life or death of biological organisms. Statistical models appropriate for any of these topics are generically called "time-to-event" models. Death or failure is called an "event", and the goal is to project or forecast the rate of events for a given population or the probability of an event for an individual.
Reliability theory of aging provides an optimistic perspective on the opportunities for healthy life-extension. According to reliability theory, human lifespan is not fixed, and it could be further increased through better body maintenance, repair, and replacement of the failed body parts in the future.
Modeling a human being as a collection of many, many redundant parts (representing cells, or clusters of cells) produces results that match the observed demographics of aging and life expectancy very well. This approach is further supported by the observed benefits of increased autophagy and apoptosis on health and longevity.
Autophagy is, broadly speaking, the process by which your cells recycle damaged components. Cells are packed full of building blocks dedicated to specific tasks, and few of them are designed to last. The average cell is a little powerhouse of dynamic destruction and construction, tearing down and rebuilding organelles left and right.
Apoptosis is the process of programmed cell death that may occur in multicellular organisms. Biochemical events lead to characteristic cell changes and death.
Both autophagy and apoptosis act to remove broken components of the body before they can cause harm. If either process is globally impaired, then the result is what amounts to faster aging: a more rapid accumulation of cellular damage that then itself causes further damage. Not a good thing. Unfortunately, impairment of apoptosis is exactly what we see in aging, as a recent review paper notes.
Apoptosis is the guardian of tissue integrity by removing unfit and injured cells without evoking inflammation. However, apoptosis seems to be a double-edged sword since during low-level chronic stress, such as in aging, increased resistance to apoptosis can lead to the survival of functionally deficient, post-mitotic cells with damaged housekeeping functions. [These] senescent cells are remarkably resistant to apoptosis, and several studies indicate that [immune system actions] can enhance anti-apoptotic signaling, which subsequently induces a senescent, pro-inflammatory phenotype during the aging process. ... We will discuss the molecular basis of age-related resistance to apoptosis and emphasize that increased resistance could enhance the aging process.
Given all the evidence, the role of immune system dysfunction (and the resulting chronic inflammation it causes) in aging appears to be fairly important. It causes disarray in many of the important biological processes that evolved to keep our bodily systems running well, and this and other contributions to degenerative aging eventually add up to bring frailty and then death.
Can autophagy and apoptosis be enhanced in the near future to bring general benefits to health and longevity? Quite possibly: calorie restriction mimetic research may eventually result in designer drugs intended to enhance autophagy, given the importance of autophagy to the benefits produced by calorie restriction. You might look at the work on spermadine as an example of a first step along this path. Conceptually similar work on apoptosis takes place in the cancer research community, where apoptosis is viewed as a dominant mechanism of cancer suppression. The bottom line is that these are signaling challenges: the body is capable of boosted autophagy and apoptosis in response to certain environment conditions, and researchers can in principle learn how to issue the signals to trigger that same boost without unwanted side-effects.
Regardless, it is true that aging is marked by uneven changes in many complex, interacting processes - such as the immune system's response to circumstances, programmed cell death signaling, and other related line items. Nothing is simple when you're down at the level of signaling systems and cells, and it's easy for the eyes to glaze over when reading the latest research and trying to put it into context. This is where good models such as the reliability theory approach to aging can help: aging is, quite clearly, a matter of accumulating damage and failing redundancy in the components of our body. Bear that in mind, and you can't go too far wrong while thinking about the latest research results.