What is cellular senescence explain the mechanism?

Cellular senescence is defined as irreversible cell cycle arrest driven by a variety of mechanisms, including telomere shortening, other forms of genotoxic stress, or mitogens or inflammatory cytokines, that culminate in the activation of the p53 tumor suppressor and/or the cyclin-dependent kinase inhibitor p16.

What are the mechanisms and functions of cell senescence?

By imposing a growth arrest, senescence limits the replication of old or damaged cells. Besides exiting the cell cycle, senescent cells undergo many other phenotypic alterations such as metabolic reprogramming, chromatin rearrangement, or autophagy modulation.

What are the four kinds of senescence?

Thus, cellular senescence might participate in four complex biological processes (tumor suppression, tumor promotion, aging, and tissue repair), some of which have apparently opposing effects. The challenge now is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks.

What are the three main points of senescence?

Senescence occurs in three different scenarios: senescence due to normal aging; senescence due to age-related diseases, and senescence induced due to therapy (such as chemotherapy).

What are the signaling pathways that lead to cellular senescence?

There are several reported signaling pathways that lead to cellular senescence including the p53 and p16 Ink4a pathways. Both of these pathways are activated in response to cellular stressors and lead to cell cycle inhibition. p53 activates p21 which prevents deactivates cyclin-dependent kinase 2 (Cdk 2).

How is the activated Notch pathway related to cell senescence?

Several common modes of regulation are listed here: Recent studies have found that the activated NOTCH pathway can block cell senescence signaling pathway by increasing the transcriptional block of the target gene HES1. So, it promotes the occurrence of cell senescence escape.

How are cell senescence and telomere damage related?

Cellular senescence caused by stress, especially epithelial cells, is mainly through the P16Ink4a/Rb pathway, while telomere-damaged senescent cells are specific, and function mainly in the mouse through the P19Arf/P53/P21Cip1 pathway. Human cells are co-regulated by two pathways.

How does blocking in the G1 phase cause cell senescence?

Blocking in the G1 phase causes cell senescence. When P21Cip1 is stressed, it can also directly cause cell growth arrest, and cells that are only regulated by the P53/P21Cip1 pathway can continue to grow after the P53/P21Cip1 pathway is turned off, while the senescent cells choose to permanently or temporarily grow stagnant.