Reviewing the reviews

A few noteworthy reviews from the previous week.

IGF signaling, mitochondria, and CR: The trifecta of aging in Caenorhabditis elegans, Wolff and Dillin:

Insulin signaling, mitochondrial respiration, and dietary restriction share conserved roles not only in the regulation of lifespan, but also in the timing and control of diverse functions such as reproduction, stress resistance and metabolism. These autonomous pathways differ in their dependence on known transcription factors and in their temporal requirements, but converge to manipulate the core set of physiological systems necessary for extended lifespan in worms. …

Mitochondria and oxidative damage: Mitochondrial respiration and reactive oxygen species in C. elegans, Sedensky and Morgan:

… The nematode Caenorhabditis elegans represents a superb model system in which to study the effects of mitochondrial function on longevity. Several mutant strains have been identified that indicate that mitochondrial function is a major factor affecting the organism’s lifespan. Taken as a group, these mutant strains indicate that metabolic rate, per se, only affects longevity indirectly. …

Systems biology: Cellular networks and the aging process, Csermely and Soti:

… we suggest a ‘weak link theory of aging’ linking the random damage of the network constituents to the overwhelming majority of the low affinity, transient interactions (weak links) in the cellular networks. We show that random damage of weak links may lead to an increase of noise and an increased vulnerability of cellular networks, and make a comparison between these predictions and the observed behaviour of the emergent properties of cellular networks in aged organisms.

Nuclear architecture and senescence: Aging: Progeria and the Lamin Connection, Kudlow and Kennedy:

The relationship between progerias — diseases that resemble premature aging — and the normal aging process has been a source of debate in the aging research community. A recent study finds that LMNA, a gene targeted for mutation in Hutchinson Gilford Progeria Syndrome, may control the onset of aging-associated decline in normal fibroblasts.

OK, I didn’t so much review them as list them. Then again, it’s a Monday.