A number of researchers are very interested in exploring differences in life span between species as a way to better understand the biology of aging; this is another branch of the mainstream interest in uncovering ways to manipulate genes and metabolism to slow aging. Amongst these scientists is Joao de Magalhaes, who runs the excellent senescence.info websites, including the GenAge and AnAge databases. You should certainly browse through the materials there if you haven't already done so. You might recall that de Magalhaes was also amongst those attempting to raise funds for genetic sequencing of long-lived mammals - again with the aim of learning more about the roots of longevity by way of comparison between species with very different life spans.
There is a good set of data showing a strong correlation between mammalian life span and the composition of mitochondrial DNA - implying that the mitochondrial free radical theory of aging in fact describes the dominant process of degenerative aging in mammals. This fits in with the clear importance of autophagy, as autophagy is the process by which damaged mitochondria are recycled before they can cause more harm to a cell and the surrounding tissue.
Here, however, let me point out a paper by de Magalhaes and other respected names in the field that looks into resistance to inflammation as a possible factor to explain life span differences between species:
Species differences in lifespan have been attributed to cellular survival during various stressors, designated here as 'cell resilience'. In primary fibroblast cultures, cell resilience during exposure to free radicals, hypoglycemia, hyperthermia, and various toxins has shown generally consistent correlations with the species characteristic lifespans of birds and mammals. However, the mechanistic links of cell resilience in fibroblast cultures to different species lifespans are poorly understood.
We propose that certain experimental stressors are relevant to somatic damage in vivo during inflammatory responses of innate immunity, particularly, resistance to ROS, low glucose, and hyperthermia. According to this hypothesis, somatic cell resilience determines species' differences in longevity during repeated infections and traumatic injuries in the natural environment. Infections and injury expose local fibroblasts and other cells to ROS generated by macrophages and to local temperature elevations. Systemically, acute phase immune reactions cause hypoglycemia and hyperthermia. We propose that cell resilience to somatic stressors incurred in inflammation is important in the evolution of longevity and that longer-lived species are specifically more resistant to immune-related stressors.
Inflammation as it applies to aging is also tied in with the degeneration of the immune system. As the immune system suffers damage and misconfiguration over the years, levels of chronic inflammation rise. In effect the immune system becomes more active, with all of the additional stress put upon the body that implies, but provides fewer benefits. This characteristic process is called inflammaging; it is plausible that a species capable of better resisting the consequences of inflammaging, as well as the consequences of inflammation in earlier life, would live longer as a result.
Finch CE, Morgan TE, Longo VD, & de Magalhaes JP (2010). Cell resilience in species lifespans: a link to inflammation? Aging cell PMID: 20415721