If you want a taste of present opinions and debates within the scientific community on any given topic, run a search of the past couple of months of publications at PubMed. It helps to have general background knowledge of the field in question, not to mention an appreciation for the nature of science and research at the leading edge, but there's always something new to learn. Here are some of the results obtained by searching on "aging longevity" and "molecular damage aging":
Traditional categorization of theories of aging into programmed and stochastic ones is outdated and obsolete. Biological aging is considered to occur mainly during the period of survival beyond the natural or essential lifespan (ELS) in Darwinian terms. Organisms survive to achieve ELS by virtue of genetically determined longevity assuring maintenance and repair systems (MRS). Aging at the molecular level is characterized by the progressive accumulation of molecular damage caused by environmental and metabolically generated free radicals, by spontaneous errors in biochemical reactions, and by nutritional components. Damages in the MRS and other pathways lead to age-related failure of MRS, molecular heterogeneity, cellular dysfunctioning, reduced stress tolerance, diseases and ultimate death. A unified theory of biological aging in terms of failure of homeodynamics comprising of MRS, and involving genes, milieu and chance, is acquiring a definitive shape and wider acceptance. Such a theory also establishes the basis for testing and developing effective means of intervention, prevention and modulation of aging.
A very dry way of jumping right on in to say that a SENS-like approach is a sensible next step if you buy in to a reliability theory view of aging - i.e. that aging is no more nor less than an accumulation of varied forms of molecular and cellular damage in a complex biological machine, and that we can work to understand and find ways to repair that damage. By repairing the damage, we prevent and reverse aging.
Various molecular and cellular alterations to our tissues accumulate throughout life as intrinsic side-effects of metabolism. These alterations are initially harmless, but some, which we may term "damage", are pathogenic when sufficiently abundant. The slowness of their accumulation explains why decline of tissue and organismal function generally does not appear until the age of 40 or older. Aging is thus best viewed as a two-part process in which metabolism causes accumulating damage and sufficiently abundant damage causes pathology. Hence, a promising approach to avoiding age-related pathology is periodically to repair the various types of damage and so maintain them at a sub-pathogenic level. Some examples of such types of damage are intracellular and others extracellular. Several types of intracellular damage are highly challenging--sophisticated cellular and genetic therapies will be needed to combat them, which are surely at least 20 years away and maybe much more. Extracellular damage, by contrast, generally appears more amenable to pharmaceutical repair which may be feasible in a shorter timeframe. In this article, the major types of age-related extracellular damage and promising avenues for their repair are reviewed.
One form of extracellular damage is the accumulation of advanced glycation endproducts, or AGEs. This is the sort of purely chemical problem that could be addressed by the existing pharmaceutical research and development infrastructure, within the present very limiting regulatory straitjacket, and more rapidly than many other aspects of aging that will require new technologies or research communities to be developed.
Moving on, we find another confirmation of one of the steps in the present form of the mitochondrial free radical theory of aging, which describes how mutated mitochondria take over cells and turn them into exporters of damaging free radicals - and how those free radicals lead to age-related disease and damage to other systems in the body.
the accumulation of acquired mutations to functionally relevant levels in aged tissues seems to be a consequence of clonal expansions of single founder molecules and not of ongoing mutational events.
The clonal expansions of damaged mitochondria occur because some types of damage prevent the cell from flagging that particular mitochondrion for destruction in the lysosome. When it comes time to repopulate after a cycle of tearing down old mitochondria, the new ones are cloned from the old - after a few cycles of this, the bad non-recycleable mitochondria take over the cell ... and then matters go south from there. Hence "clonal expansion" - the population of bad mitochondria in a cell expands through cloning.
If you're up for something a little more dense, here is more on naked mole rat biochemistry; in essence it recapitulates what has been said in the popular science press - naked mole rats produce lots of free radicals, but don't appear to be suffering anywhere near the same level of consequences to cellular components, health and life span that other rodents do.
Vascular aging is characterized by decreased nitric oxide (NO) bioavailability, oxidative stress, and enhanced apoptotic cell death. We hypothesized that interspecies comparative assesment of vascular function among rodents with disparate longevity may offer insight into the mechanisms determining successful vascular aging. ... Interspecies comparison showed there is a negative correlation between H(2)O(2)-induced apoptotic cell death and [maximum life span]. Thus endothelial vasodilator function and vascular production of reactive oxygen species do not correlate with maximal lifespan, whereas increased lifespan potential is associated with an increased vascular resistance to proapoptotic stimuli.
One theory advanced is that it has to do with the proportionality of various species of lipid, the biochemicals in which such damage is most consequential to your heath. It seems that naked mole rats have more of the resistant lipids and less of the easily damaged lipids.
Lastly, a reminder that senescent cells are most likely not good for you:
The second type of supernumerary cells, senescent cells, accumulate in quite large numbers in one tissue, the cartilage in our joints. They also accumulate elsewhere, but in much smaller numbers; however, these may still be important by being actively toxic. They aren't able to divide when they should, and they also secrete abnormally large amounts of some proteins.
Cellular senescence, a stress induced growth arrest of somatic cells, was first documented in cell cultures over 40 years ago, however its physiological significance has only recently been demonstrated. Using novel biomarkers of cellular senescence we examined whether senescent cells accumulate in tissues from baboons of ages encompassing the entire lifespan of this species. We show that dermal fibroblasts, displaying markers of senescence such as telomere damage, active checkpoint kinase ATM, high levels of heterochromatin proteins and elevated levels of p16, accumulate in skin biopsies from baboons with advancing age. The number of dermal fibroblasts containing damaged telomeres reaches a value of over 15% of total fibroblasts, whereas 80% of cells contain high levels of the heterochromatin protein HIRA.
If a function or population within the body differs between youth and age, then that is something researchers need to look at: is a root cause or consequence of aging? If the former, then we should aim to do something about it.