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A decline in cell function with advancing age is a ubiquitous characteristic of all organisms.
In these two cell types, PA led to a significant dose- and time-dependent decline in cell function and survival.
We have previously reported that liver of old mice have increased cysteine oxidation (Zhang et al. 2007) that parallels age-related dysfunction of mitochondria and is thought to be a major determinant of this decline in cell function, since these organelles are both the main sources of reactive oxygen species (ROS) and targets for their damaging effects (Lanza and Nair 2012).
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Previous studies have shown that there is an age-related decline in cell functions [ 37– 40].
By contrast, clinical observations indicate that the pain of chronic pancreatitis will occasionally decline in parallel with a decline in acinar cell function, possibly due to the 'burn-out' of residual acinar cells (Sakorafas et al., 2007).
Although the effects of aging on B-lymphopoiesis differ between mice and humans, there is significant overlap in the decline in B cell function found in aged population from both species.
The pathology of type 2 diabetes comprises initial hyperinsulinaemia with, thereafter, a continuous decline in beta cell function in association with a progressive decrease in beta cell mass due to an increasing rate of beta cell apoptosis [ 3].
This suggests a rapid decline in beta cell function in them and that beta cell failure is a predominant feature in our patients with type2 diabetes.
Importantly, a number of experimental studies have shown that the age-associated DNAm changes seen in stem cells may underlie the observed decline in stem cell function, for instance in the case of MSCs (53) and myogenic stem cells (54).
During aging, a decline in stem cell function is observed in many tissues.
In this regard, a recent report has described the causal involvement of inflammatory pathways in the age-related decline in stem cell function [ 6].
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