Two recent reviews discuss the evidence that mitochondria (specifically, age- and damage-related dysfunction in these organelles) are responsible for age-related degenerative conditions. Both reviews focus on oxidative stress as a primary mechanism underlying the connections, but depending on the disease in question, they reach rather different conclusions about the significance of mitochondrial damage.

Kim et al. describe the role for mitochondria (in particular, reactive oxygen species [ROS] produced by damaged mitos and the concomitant inflammation) in the etiology of late-life insulin resistance. The authors conclude that the balance of evidence supports a role for mitochondrial damage in late-onset diabetes, and I think their arguments are reasonable (though I’m hard pressed to think of a phenomenon that doesn’t play some role in diabetes).

Meanwhile, Fukui and Moraes critically evaluate the idea that ROS-induced damage causing further ROS production, and the possibility that such a “vicious cycle” could participate in the development of neurodegenerative diseases. Their conclusion is that the field has been led astray by results of in vitro experiments that don’t accurately model the situation in vivo.