By way of Ouroboros we learn of a new open access journal on aging science, titled AGING. I'm always pleased to see the spread of open access science in the areas I'm interested in: it heralds faster research as barriers to the spread and analysis of knowledge are lowered.
AGING publishes high-impact research papers of general interest and biological significance in all fields of aging research including but not limited to cellular senescence, DNA damage and repair, organismal aging, age-related diseases, genetic control of aging from yeast to mammals, regulation of longevity, evolution of aging, anti-aging strategies and drug development and especially the role of signal transduction pathways in aging and potential approaches to modulate these signaling pathways to extend lifespan.
In the first issue, there are a couple of items of interest, amongst them a review paper on chromatin modifications and aging. This is a topic that has cropped up before, and is an aspect of epigenetics in aging:
Strictly speaking, 'epigenetics' refers to chromatin and DNA modifications that are heritable through cell division, but do not involve changes in the underlying DNA sequence ... Chromatin structure is not fixed. Instead, chromatin is dynamic and is subject to extensive developmental and age-associated remodeling. In some cases, this remodeling appears to counter the aging and age-associated diseases, such as cancer, and extend organismal lifespan. However, stochastic non-deterministic changes in chromatin structure might, over time, also contribute to the break down of nuclear, cell and tissue function, and consequently aging and age-associated diseases.
It's all still somewhat up in the air as to what is causing what with respect to chromatin changes, and this biochemistry is very complex. But take a look at the paper and see what you think.
It has been well recognized that, as the mammalian cell ages, its chromatin structure evolves, both at a global level and at specific loci. While these observations are mostly correlative, recent technical developments allowing loss-of-function experiments and genome-wide approaches have permitted the identification of a causal relationship between specific changes in chromatin structure and the aging phenotype. Here we review the evidence pointing to the modulation of chromatin structure as a potential driving force of cellular aging in mammals.
if chromatin modifiers can directly contribute to the aging phenotype, what is the molecular circuitry leading to the modulation of their activities during the aging process, and may it be altered as a therapeutic means?