The present case demonstrated significant pathology in the adjoining mucosa, which pointed toward a replicative senescence
Antioxidants inhibit nuclear export of telomerase reverse transcriptase and delay replicative senescence
of endothelial cells," Circulation Research, vol.
In fact, the TL in acrolein-treated cells at 30 PD was similar to that in control cells at 46 PD, when normal replicative senescence
The role of CD8+ T-cell replicative senescence
in human aging.
This special aspect of cellular senescence is known as replicative senescence
It has therefore been proposed that telomeres could be an important part of an internal "clock" mechanism that may account for replicative senescence
Therefore, there is great need to identify methods to prevent oxidative stress and replicative senescence
However, during chronic HIV-1 infection, CD8+ T-cells exhaust their ability to up-regulate telomerase, leading to critically short telomeres and other changes associated with replicative senescence
(cellular aging), reducing their antiviral activity.
Lately, miR-760 and miR-186 upregulation has been associated with replicative senescence
in human lung fibroblast cells.
of T cells: does the Hayflick Limit lead to immune exhaustion?
As HIV disease progresses, certain immune cells called CD8 cytotoxic T-cells undergo accelerated replicative senescence
(cellular aging) and lose their ability to proliferate and kill HIV-infected CD4 T-cells.
Primary cultured cells undergo replicative senescence
, which is characterized by telomere shortening, genomic damage, epigenomic damage, and activation of tumor suppressors .
Alterations of proteasome function have been recorded in various biological phenomena including ageing and replicative senescence
During the progression of HIV disease, certain immune cells called CD8+ cytotoxic T-cells undergo accelerated replicative senescence
(cellular aging), and lose their ability to proliferate and kill HIV-infected CD4+ T-cells.
The results show that replicative senescence
results in reduced capacities of myoblasts to differentiate, in association with defective glycose and lipid metabolism, decreased cellular mitochondrial and ATP contents, and increased ROS production, these changes accompanied with normal-to-increased ATP synthesis capacities of mitochondria [32, 33].