Aging is frequently viewed, albeit with inadequate logical justification, as solely the result of "wear and tear", as though it were a set of generic processes, intrinsic to the passage of time.
Bluntly, this point of view suggests that we get old because we "wear out".
The stance is often assumed to be obvious, self-explanatory, and without any need for support, logical or factual.
Accurate within a very narrow conceptual domain, the view is nonetheless parochial and fails when applied in a wider biological framework.
It cannot explain aging – and the lack of aging – in any but the most common organisms.
Even in such common organisms – for example, humans and mice – the view is neither robust nor consistent with known pathology and is incompatible with current data on germ cell survival, cancer, and telomere biology.
To achieve an accurate understanding of aging, wear and tear is almost certainly necessary but certainly not sufficient.
Many cell lines and some multicellular organisms demonstrate indefinite maintenance in the face of such wear and tear, showing no accumulation of dysfunction.
This is true of such cell lines as germ cell lineages, cancer cells, and telomerized human somatic cells.
It is arguably true of some multicellular organisms such as the hydra.
Despite the "slings and arrows" of a perennially hostile environment, there is a notable lack of aging in these cases.
While it may be roughly accurate to say that homeostasis routinely wanes in most cell lines and in the majority of multicellular organisms (that is, most cell lines and most organisms age), a comprehensive understanding of aging requires that we explain the exceptions as well.
We must account for both the maintenance of indefinite cellular and organismal homeostasis (that is, the lack of aging) and its far more common failure (that is, aging).
Moreover, current laboratory evidence suggests that we might take lessons from the former and apply them to the latter with potentially unprecedented clinical benefits.
Specifically, we may be able to take cells that would normally age and induce them to remain immortal by using the same mechanisms employed in, for example, germ cell lines and cancer cells.
Maintaining indefinite cellular homeostasis is not so much a matter of redesigning cells as it is of adjusting their genetic expression.
In the case of cells in vitro and in vivo, and in the case of reconstituted human tissue ex vivo, preventing aging is not a matter of replacing genes, but simply a matter of altering gene expression of those genes the cell normally possesses.
Indefinite maintenance of cellular function in the face of continual damage is a remarkably reliable biological phenomenon.
It occurs in the germ cell lines of organisms whose somatic cells show aging changes, again suggesting that cellular aging may be not so much a matter of having the wrong genes as it is of expressing the ones you have poorly.
Aging results from bad gene expression, not bad genes.
The lessons of gene expression that we learn from understanding cellular senescence may be taken into clinical medicine, allowing us to prevent and treat the diseases of aging and, perhaps, aging itself.