The SENS model of aging, and the resulting research programs aimed at producing rejuvenation treatments, are predicated on identifying the forms of cellular and tissue damage that are the initial, primary cause of aging. This means damage that occurs directly as a result of the normal operation of healthy metabolism, and excludes damage that occurs as a secondary consequence of other forms of damage. There is arguably a far greater variety of secondary damage than primary damage, which is only to be expected given the complexity of living organisms. Simple damage in a complex system produces complex results. This is why SENS can be viewed as a shortcut to meaningful results in treating aging: it is focused on a narrow, fairly well understood, and simpler region of our biology. The hope is that in repairing the primary forms of damage, most of the secondary forms of damage will then be repaired by our own maintenance mechanisms.
You don't have to dive too far into the research literature to find grey areas and unknowns, however. There are a number of forms of damage that could be either primary or secondary harms, and finding out which is the case still lies somewhere in the future. If funding for SENS research was far greater than it is now, then it would make sense to open repair programs for all of the ambiguous forms of damage: err on the side of caution and fix everything. Since funding is still minimal, however, the most cost-effective path is to work on fixing the definitive forms of primary damage and then see how that affects other forms of damage and change that occur in aging.
Q: A lot of tissues, including notably the arteries, develop calcium deposits with age. Isn't this also an important kind of aging damage? Don't you need to develop a new rejuvenation biotechnology to remove it from our tissues?
A: To answer the question, we first need to disaggregate (no pun intended) the general category of "calcification." There are quite a few tissues that calcify to some degree in most or all aging people, and the reasons why this occurs and the nature of the structural disruption it causes are quite distinct depending on the tissue. In fact, even looking at just the arteries, there are several different kinds of "arterial calcification," including calcification connected with atherosclerotic plaque and calcification of the fibrils of elastin protein that loan the arteries their elasticity.
It's unlikely that all of these are true aging damage, but it's quite plausible that at least some of them are. The key question is whether each of these calcified deposits are really an intrinsically more or less irreversible change, or if like many other things that go wrong in aging they're sufficiently dependent on other, primary age-related changes that they would revert to the healthy norm if the original insult were resolved. In the former case, we would indeed need to develop rejuvenation biotechnologies to remove them. But it seems likely that some forms of age-related tissue calcification occur and are sustained by the effects of other forms of aging damage or the body's responses to them - things like oxidative stress caused by accumulation of cells that have been taken over by mutant mitochondria, or the inflammatory secretions of senescent cells. If calcification is driven and perpetuated by the effects of other, primary kinds of aging damage, then all we will really have to do is remove or repair the original aging damage, and the downstream calcification will resolve itself "for free" (or the body's natural repair and maintenance machinery will do it for us).
The more well-understood form of arterial calcification, for instance, is pretty clearly a secondary effect of local atherosclerotic lesions, and driven by inflammation. Once we clear the oxidized cholesterol products from atherosclerotic foam cells and allow them to egress, the body's wound-healing response will cease to play its perverse role in perpetuating and complicating the lesion but will instead begin resolving and repairing the damage wrought in the artery wall. Under those conditions, the calcium deposits may well simply dissolve, or resolve as local cells are no longer being pushed (as they often are in atherosclerotic lesions) into adopting behaviors that closer resemble those of bone-forming cells.
Ultimately, barring strong evidence coming in one way or the other, the best policy is to remain agnostic about such cases, and focus precious research investments on those therapies that target the clearly-identified, recalcitrant cellular and molecular damage of aging. Like many types of secondary damage, other forms of tissue calcification may similarly become a non-issue once we've taken care of the core damage driving degenerative aging. If this turns out to be the case, calcification-specific rejuvenation biotechnologies will not be necessary.