I chose this article because of the authors of “Why we get sick” talked about senescence. So, it sparked my interest.
This article talks about cell signaling networks and mechanisms that underly the types of cellular senescence. Senescence is a process where cells cease dividing and undergo distinctive phenotypic alterations, such as chromatin and secretome changes, and tumor-suppressor activation. Cellular senescence, while having been known to have irreversible cell-cycle arrest mechanisms acting to protect us from cancer, more recently have been shown to have a role has in assisting processes such as development, tissue repair, aging and age-related disorders.
This article talks about cell signaling networks and mechanisms that underly the types of cellular senescence. Senescence is a process where cells cease dividing and undergo distinctive phenotypic alterations, such as chromatin and secretome changes, and tumor-suppressor activation. Cellular senescence, while having been known to have irreversible cell-cycle arrest mechanisms acting to protect us from cancer, more recently have been shown to have a role has in assisting processes such as development, tissue repair, aging and age-related disorders.
This figure shows a variety of cell extrinsic and intrinsic stressors that can activate the cellular senescence program.
This figure shows the hypothetical multi-step senescence model showing evidence that cellular senescence can be driven by epigenetic and genetic changes. Progression to deep or late senescence may be driven by additional genetic and epigenetic changes, like chromatin budding, histone proteolysis and retrotransposition. These changes can be the driving force for further transcriptional change and senescence-associated secretory phenotype (SASP) heterogeneity (yellow, magenta, pink and blue dots). SASP is key in that it distinguishes cells from quiescent, terminally differentiated and other types of non-proliferating cells.
Senescent cells are subdivided into two main classes based upon the kinetics of senescence induction and their functionality. Acute senescent cells are tightly orchestrated biological processes that can be representative of a wound healing, tissue repair, embryonic development. These processes halt expansion of certain cells and produce a SASP with defined paracrine functions. On the other other-hand chronic senescence is not programmed and does not target specific cell types, rather occurs due to age-related immunodeficiency or production of less proinflammatory SASPs.
Warrenkevin Henderson
Potluck 13APR20
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214092/
This figure shows the hypothetical multi-step senescence model showing evidence that cellular senescence can be driven by epigenetic and genetic changes. Progression to deep or late senescence may be driven by additional genetic and epigenetic changes, like chromatin budding, histone proteolysis and retrotransposition. These changes can be the driving force for further transcriptional change and senescence-associated secretory phenotype (SASP) heterogeneity (yellow, magenta, pink and blue dots). SASP is key in that it distinguishes cells from quiescent, terminally differentiated and other types of non-proliferating cells.
Senescent cells are subdivided into two main classes based upon the kinetics of senescence induction and their functionality. Acute senescent cells are tightly orchestrated biological processes that can be representative of a wound healing, tissue repair, embryonic development. These processes halt expansion of certain cells and produce a SASP with defined paracrine functions. On the other other-hand chronic senescence is not programmed and does not target specific cell types, rather occurs due to age-related immunodeficiency or production of less proinflammatory SASPs.
Warrenkevin Henderson
Potluck 13APR20
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214092/
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