Sentences with phrase «secretory phenotypes»

«Senescence - associated secretory phenotypes reveal cell - nonautonomous functions of oncogenic RAS and the p53 tumor suppressor.»

Laberge said the paradigm - shifting potential of intermittent dosing is based on the fact that it takes time for the inflammatory loop (fueled by the senescence - associated secretory phenotype or SASP) to form and time for it to re-establish itself after a brief treatment of rapamycin.

Masters et al. discuss the often overlooked contribution of the stromal microenvironment as an extrinsic factor to immunosenescence and inflammation.12 Accumulation of senescent stromal cells which demonstrate the senescent associated secretory phenotype (SAPS), may alter tissue structure and function, and increase local inflammation.13 The impact of altered lymphoid stromal microenvironment may be widespread and include altered haematopoiesis, reduced lymphatic flow and disrupted secondary lymphoid organisation, which consequently will alter antigen transportation and presentation to T cells.12

A late stage treatment may help with some inflammation associated with the senescence - associated secretory phenotype (increased inflammation, MMPs, etc.) but it likely won't be as effective as preventing the aging - related damage in the first place.»

* The principle caveat would be that the interaction of senescence with defective mitotic checkpoint function within such cells, and the effects upon their neighbors of their state and of their senescence - associated secretory phenotype, would very likely cause some phenomena that would not be observed in p16Ink4a - senescent cells or in their effects on neighbors.

Control of the senescence - associated secretory phenotype by NF --LCB- kappa -RCB- B promotes senescence and enhances chemosensitivity.

Persistent DNA damage and DDR signaling triggers senescent cells to secrete immunomodulatory proteins, a phenomenon known as the senescence - associated secretory phenotype (SASP).

Health improvement (allowing to post - pone / escape the diseases and thus live, healthier / disease - free longer, but not above human MLSP of around 122 years; thus these therapies do not affect epigenetic aging whatsoever, they are degenerative aging problems not regular healthy aging problem (except OncoSENS - only when you Already Have Cancer - which cancer increases epigenetic aging, but cancer removal thus does not change anything / makes no difference about what happens in the other cells / about what happens in the normal epigenetic «aging» course in Normal non-cancerous healthy cells) Although there is not such thing as «healthy aging» all aging in «unhealthy» (as seen from elders who are «healthy enough» who show much damage), it's just «tolerable / liveable» enough (in terms of damage accumulating) that it does not affect their quality of life (enough yet), that is «healthy aging»: ApoptoSENS - Clearing Senescent Cells (this will have great impact to reduce diseases, the largest one, since it's all inflammation fueled by the inflammation secretory phenotype (SASP) of these senescent cells) AmyloSENS - Dissolving the Plaques (this will allow humans to evade Alzheimer's, Parkinsons and general brain degenerescence, allowing quite a boost; making people much more easily reach the big 100 - since the brain is causal to how long we live; keeping brain amyloid - free and keeping our memories / neuron sharp / means longer LongTerm Potentiation - means longer brain function means longer heavy brain mass (gray matter / white matter retention seen in «sharp - witted» Centenarians who show are younger brain for their age), and both are correlated to MLSP).

P Sapieha, et al (2016) Senescence - associated secretory phenotype contributes to pathological angiogenesis in retinopathy.

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.

One well - known characteristic of senescent cells is the production of pro-inflammatory and matrix - degrading molecules, known as the senescence - associated secretory phenotype (SASP).

Senescent cells may promote tumour progression through the activation of a senescence - associated secretory phenotype (SASP), whether these cells are capable of initiating tumourigenesis in vivo is not known.

Previous work has revealed it could impact on something called the senescence - associated secretory phenotype, or SASP.

This accelerates cell senescence, which leads to increased pro-inflammatory and pro-oxidant signaling by the senescence associated secretory phenotype (SASP) response, and induction of mitochondrial dysfunction, thereby propagating DNA damage and senescence to bystander cells.

Not exact matches

Secondly, the secretory and other phenotypes of such cells progressively derange local and systemic metabolism and tissue function, rendering tissues more vulnerable to metastasis, promoting systemic inflammation, and otherwise impairing tissue function.