Amongst the figures of the aging research community - which is pretty much still so small that everyone knows everyone else - there is one fairly prolific author of papers who argues that the mTOR gene is a major regulator of aging. This is an example of someone who sees aging as largely programmed rather than the result of stochastic damage at the level of cells and cellular protein machinery. I think that those folk have a tall hill to climb in order to make their case, based on present evidence, and this particular mTOR specialist might be seeing nails everywhere when the tool to hand is a hammer. But intelligent people can differ, and an important part of reading the scientific literature is to understand that there are ongoing and important differences of opinion under the hood - points are being argued, and most of those positions will ultimately be shown to be incorrect in some way, shape, or form.
In this open access paper, the fellow outlines his view of cellular senescence and how it emerges from a cell that has entered cell cycle arrest due to failing its checkpoints. You'll recall that cellular senescence is the fate awaiting old cells that someone are not removed - either by destroying themselves or being destroyed by the immune system. They are damaging to surrounding tissue and contribute to degenerative aging; their numbers grow rapidly in advanced age, probably due to decline in other systems and a rising level of damage in the body. The paper quoted below is educational and well worth reading, while bearing in mind that the overall case that he makes with regard to mTOR and programmed aging seems weak on the face of it.
Cell cycle arrest is not yet senescence. When the cell cycle is arrested, an inappropriate growth-promotion converts an arrest into senescence (geroconversion). ... As discussed in the article, cell cycle arrest is not yet senescence and senescence is not just arrest: senescence can be driven by growth-promoting pathways such as mTOR, when actual growth is impossible. ... This mechanism connects cellular senescence, organismal aging and age-related diseases.
You might notice that an accumulation of molecular damage was never mentioned in this article. It was unneeded. Cellular aging and geroconversion is not caused by accumulation of random molecular damage. Although damage accumulates, I suggest that the organism does not live long enough to suffer from this accumulation
One definition of organismal aging is an increase in the probability of death. Gerogenic cells (due to their hyper-activity and signal-resistance) may slowly cause atherosclerosis, hypertension, insulin-resistance, obesity, cancer, neurodegeneration, age-related macular degeneration, prostate enlargement, menopause, hair loss, osteoporosis, osteoarthritis, benign tumors and skin alterations. These conditions lead to damage - not molecular damage but organ and system damage. Examples include beta-cell failure, ovarian failure (menopause), myocardial infarction, stroke, renal failure, broken hips, cancer metastases and so on. These are acute catastrophes, which cause death. I suggest that by suppressing geroconversion, gerosuppressants will prevent diseases and extend healthy life span.
The part that stands out to me is this:
Cellular aging and geroconversion is not caused by accumulation of random molecular damage.
That is a claim that I think is already readily refuted by the available evidence. But don't let that stop you reading the paper; it's an interesting view on the accumulation of senescent cells, which are demonstrated to be an important factor in aging and worthy of more research attention - they do in fact contribute to the long list of conditions provided by the author above, and more besides.