Cellular senescence and the senescent secretory phenotype: therapeutic opportunities

Клеточное старение и секреторный фенотип стареющих клеток: терапевтические возможности
Judith Campisi, Tamar Tchkonia, James L. Kirkland, Yi Zhu, Jan van Deursen
2013-03-01

age-related diseasescellular senescencechronic inflammationsenescence-associated secretory phenotypesenescent cells
Aging is the largest risk factor for most chronic diseases, which account for the majority of morbidity and health care expenditures in developed nations. New findings suggest that aging is a modifiable risk factor, and it may be feasible to delay age-related diseases as a group by modulating fundamental aging mechanisms. One such mechanism is cellular senescence, which can cause chronic inflammation through the senescence-associated secretory phenotype (SASP). We review the mechanisms that induce senescence and the SASP, their associations with chronic disease and frailty, therapeutic opportunities based on targeting senescent cells and the SASP, and potential paths to developing clinical interventions.
1
Aging may be a modifiable risk factor, potentially allowing multiple age-related diseases to be delayed by targeting fundamental aging mechanisms.
2
Cellular senescence and the SASP are associated with chronic disease and frailty.
3
Cellular senescence contributes to chronic inflammation through the senescence-associated secretory phenotype (SASP).
4
Developing clinical interventions will require translating mechanistic insights about senescence and the SASP into actionable therapies.
5
Therapeutic strategies may target senescent cells or the SASP to prevent or treat age-related pathology.

Cellular senescence and the senescence-associated secretory phenotype (SASP)

The mechanisms inducing cellular senescence and the SASP, their associations with chronic disease and frailty, and therapeutic opportunities for targeting senescent cells and the SASP

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2013-03-01
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Judith Campisi
Tamar Tchkonia
James L. Kirkland
Yi Zhu
Jan van Deursen
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