Back in 2008 or so, a group of researchers crunched the numbers to argue that most of the variation in longevity between mammal species (which spans the range from small rodents that live a couple of years to whales that live a couple of centuries) is largely determined by resting metabolic rate and variations in mitochondrial DNA. Our mitochondria are the power plants of the cell, the descendants of symbiotic bacteria with their own DNA, and they toil to produce chemical energy stores to power the rest of the cell machinery. They occupy a central role in our biology, and this is one of many papers that point to the significance of mitochondria in aging.
For an introduction on why mitochondria and their composition are important, you might look back in the Fight Aging! archives, or investigate the membrane pacemaker hypothesis of aging. The short version of the story is that mitochondria produce damaging reactive byproducts in the course of their operation: anything that can react with protein machinery and disrupt its operation is harmful to a cell, though most such incidences are quickly repaired. The cell components that suffers the brunt of the damage are of course the mitochondria themselves, which only makes the situation progressively worse. Some species are better at soaking up the reactive compounds with natural antioxidant proteins, while others have mitochondria and cell structures that are more resistant to damage, some can better repair damaged mitochondria, and yet more have more efficient mitochondria that emit fewer damaging molecules - all of these things tend to lead to a longer life when present.
While engineering humans to have better mitochondria is going to happen sooner or later, there are also other and arguably better near term options for dealing with the issue. A number of research groups are working towards ways to repair or replace mitochondria in living tissue, and thus removing their contribution to degenerative aging. This is a very necessary part of the rejuvenation toolkit of future medicine, but like much of the present work in this field it is poorly funded and proceeding far more slowly than it might be.
The researchers mentioned above, who investigated correlations between metabolic rate and longevity, recently published this open access paper in which there is some more number crunching to probe associations between various measures and species maximum life span (MLS):
We have previously shown that body mass (BM) or resting metabolic rate alone explain around 40-50% of the variation in mammalian longevity, whereas their combination with mitochondrial DNA (mtDNA) GC content could explain over 70% of the MLS variation. Consequently, we hypothesized that other putative players in MLS determination should have relatively small contribution or their effects should be mediated by the above factors.
Recent finding by Gomes et al. (2011) demonstrating a strong negative correlation between telomere length and MLS in 59 mammalian species calls for re-evaluation of this hypothesis. Indeed, the coefficient of MLS determination calculated using the data in their paper indicates that the telomere length could alone explain more than 1/3 of the variation in the lifespan of mammals. Here, we explore whether the telomere length has an independent impact on mammalian longevity or its effect is attributed to co-variation with other determinants of MLS, such as BM and mtDNA GC content.
Partial correlation and multivariate analyses showed that the telomere length has an independent impact on longevity determination. The partial correlation analysis allows eliminating the co-variation effects. We found that the correlative links between telomere length and BM or mtDNA GC do not significantly alter its association with longevity. That is, the telomere length could explain part of the variation in the mammalian longevity which is not explained by the BM and mtDNA GC.
In attempt to discover [other possible] still unaccounted factors, we further included in the analysis an additional variable closely related but not identical to the metabolic rate - body temperature (Tb). Gomes et al. (2011) hypothesized that the evolution from exothermic to homeothermic organisms was accompanied by telomere shortening as a tumor protective adaptation to an enhanced mutation load caused by high Tb. Yet, within mammalian species we did not observe any significant correlation between the telomere length and typical Tb.
Unexpectedly, we found that Tb [may] explain some cases of considerable deviations from the MLS predicted by BM, mtDNA GC, and telomere length. For example, the naked mole-rat (Heterocephalus glaber) and North American pika (Ochotona princeps) have similar values of BM, mtDNA GC content and telomere length, yet the naked mole-rat lives 4.4 times longer. This apparent "discrepancy" could be largely attributed to the difference in Tb which, in the sample analyzed, is the lowest for the naked mole-rat (32.1°C) and the highest for the North American pika (40.1°C).