Sentences with phrase «senescent cells in a tissue»

Larger numbers of senescent cells in a tissue make it more vulnerable to the spread of cancer, contribute to inflammation, and skew the local activity of the immune system.

Not exact matches

Senescence is associated with normal aging, and senescent cells accumulate in aged tissues, which impair the normal functions of the tissue and contribute to age - related diseases.

This series addresses the contribution of cellular senescence to cardiovascular, neurodegenerative, and arthritic disorders as well as the senescent phenotypes in various tissues and cell types.

A recent study, led by an international team of researchers confirms that targeted removal of senescent cells (SnCs), accumulated in many vertebrate tissues as we age, contribute significantly in delaying the onset of age - related pathologies.

Senescent cells have removed themselves from the cycle of replication in reaction to cell and tissue damage, or a local tissue environment that seems likely to result in cancer.

Moreover, there are yet other cell types — such as visceral adipose tissue macrophages and cytotoxic CD8 + T - cells — in which the age - related supernumerary accumulation of dysfunctional and apoptosis - resistant cells appears to play a highly deleterious role on tissue function, but where the cells are not «senescent» cells in the classical sense of p16Ink4a expression and the senescence - associated secretory profile observed in senescent fibroblasts.

On the other hand, there are many other tissues — notably, the kidney and articular cartilage — where p16Ink4a - expressing senescent cells appear to be a contributing factor to human and murine degenerative aging, but which were not evaluated in treated or control mice in this study, and it would be of interest to see the effects of ablation of p16Ink4a - positive senescent cells.

But then why do senescent cells accumulate in our tissues with age?

With their deep expertise in the biology of senescent cells, the Campisi lab will be focused on fundamental research into questions like how senescent cells vary in their susceptibility and resistance to immune clearance (depending on factors like their tissues of residence or the pathway that led them into senescence); the targets and mechanisms used by NK cells to clear senescent cells; and why subsets of senescent cells might persist when their similarly - situated neighbors are cleared out (and what might allow us to overcome that resistance).

After initial testing demonstrated that their senoablative constructs could eliminate up to 80 % of senescent cells in cell culture, the Oisín team tested them out in living mice, showing that it can purge senescent cells from multiple tissues in middle - aged animals.

To impute aging phenotypes directly to p16Ink4a - expressing senescent cells, van Deursen and colleagues with expertise in the aging and senescence of the relevant tissues developed and tested the effects of a pharmacologically - inducible system for the ablation of p16Ink4a - expressing cells.

Rather, the defective checkpoint system was left to proceed, and one of its downstream consequences, which was still under normal regulation — and one known to be directly induced by the normal degenerative aging process — was reversed at the structural level, by clearing out the p16Ink4a - positive senescent cells that had accumulated to an abnormal degree in their tissues.

In addition to halting growth, senescent cells secrete abnormally large amounts of proteins that inflame the immune system and degrade the normal supporting tissue architecture.

Senescent cells lose their normal function in the tissue, cease dividing, and begin secreting a deadly mix of inflammatory and tissue - degrading factors collectively known as the senescence - associated secretory phenotype (SASP) that damages and deranges local tissues.

As the investigators note, the rapid age - related arterial stiffening and cardiac arrhythmias that appear to be at cause for the majority of deaths in BubR1H / H mice were not attenuated by ablating p16Ink4a - expressing senescent cells — but these tissues had little burden of such cells, so this finding reinforces the conclusion that the multiple aging phenotypes arrested in these mice when senescent cells were ablated is attributable specifically to the removal of their baleful influence on local tissues.

Thus, these animals exhibit premature cardiac arrhythmias and stiffening of the arterial wall, and cardiac failure appears to be the main cause of death; yet these tissues are not burdened with an abnormally - high burden of p16Ink4a - senescent cells, and accordingly, ablation p16Ink4a - positive senescent cells in these animals had little tissue - specific or survivorship phenotypic impact.

These data indicate that cellular senescence is causally implicated in generating age - related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.

Only in the last 10 years, with increasing knowledge of the senescent phenotype and the ability to detect senescent cells in human tissues, have biologists been able to investigate the relationship between cellular senescence and disease.

An enzyme called SETD8 appears to play a critical role in cellular senescence onset Senescent cells may have stopped dividing, but they continue to remain active — churning out a specific cocktail of factors that increases inflammation and breaks down tissue among other things.