Investigating the biochemistry of aging in long-lived species and study of the impact of mitochondrial damage on aging are two quite distinct lines of research. They start to overlap on the matter of lipids, however, and the types and relative proportions of lipids that make up the membranes of cells and cellular components.
If you look back in the Fight Aging! archives, you'll find introductory entries on this topic:
You might recall that different fatty acid or lipid composition in cell membranes was floated as a reason for the ninefold longevity of naked mole-rats over related rodent species. Plenty of oxidative stress in the older mole-rats, but little sign of biochemical damage resulting from it - in comparison to those other rodents long since aged to death, that is. Better, more damage-resistant building blocks down at the molecular level might be the cause.
Better and more damage resistant building blocks: the mitochondrial free radical theory of aging paints mitochondria as the original source of damaging free radicals that react with and destroy cellular machinery - a process that ultimately contributes to age-related conditions such as atherosclerosis. If the machinery is more resistant to free radicals, then we would expect this contribution to aging to have a lesser effect, and thus lead to a longer life span.
If you dig further, you'll see that mitochondrial membrane damage is important in the mitochondrial free radical theory of aging, and the composition of mitochondrial DNA - the blueprint for the proteins that make up mitochondrial structure, such as the membranes - correlate strongly with species maximum life span.
I recently noticed an open access commentary that revisits this area of research:
Scientific investigation of mechanisms that determine lifespan can be divided into three general approaches. The first approach (the comparative method) began over a century ago comparing species differing greatly in maximum longevity and implicated a role for the speed of metabolism in determining the length of life
The recent insight from the comparative approach has been to link membrane fatty acid composition to maximum lifespan. This link grew from the finding that membrane fatty acid composition varied systematically with body-size among mammals and the suggestion this caused different cellular metabolic rates in mammals. Membrane fatty acid was then also linked to maximum lifespan (MLSP) variation among mammals. The reason why membrane fatty acid composition is correlated with MLSP is because fatty acids differ greatly in their susceptibility to lipid peroxidation.
Peroxidation of lipids in the body is effectively a form of damage: it is the reaction between a lipid and a free radical, changing the molecular structure of the lipid and rendering it unable to perform its assigned task in the cellular machinery of which it is a part. More resistant lipids means more damage-resistant mitochondria - and damage-resistant mitochondria should translate fairly directly into enhanced life span. So far the evidence supports this way of looking at matters.
That there is such a strong correlation between the building blocks of mitochondrial membranes and species life span is another strong sign that mitochondrial damage is very important in aging - and thus we should prioritize present efforts to support the development of biotechnologies that can repair or replace mitochondria throughout the body. These therapies are tantalizingly close to realization, but progress is slow and will remain slow until such time as funding and public interest are much larger than they are today.