Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 23, Pages -Publisher
MDPI
DOI: 10.3390/ijms222313173
Keywords
cellular senescence; cell cycle arrest; DNA damage signaling; transcriptome signature; senescence-associated secretory phenotype; mitochondrial dysfunction; metabolism alteration; epigenetic and chromatin changes; aging
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Cellular senescence is an essentially irreversible proliferative arrest state where cells release pro-inflammatory and proteolytic factors. Different types of senescent cells accumulate in various tissues and organs with unique functions. Understanding how cells undergo extensive changes to induce a common cellular state is crucial for cancer prevention and improving health during aging.
Cellular senescence entails a state of an essentially irreversible proliferative arrest in which cells remain metabolically active and secrete a range of pro-inflammatory and proteolytic factors as part of the senescence-associated secretory phenotype. There are different types of senescent cells, and senescence can be induced in response to many DNA damage signals. Senescent cells accumulate in different tissues and organs where they have distinct physiological and pathological functions. Despite this diversity, all senescent cells must be able to survive in a nondividing state while protecting themselves from positive feedback loops linked to the constant activation of the DNA damage response. This capacity requires changes in core cellular programs. Understanding how different cell types can undergo extensive changes in their transcriptional programs, metabolism, heterochromatin patterns, and cellular structures to induce a common cellular state is crucial to preventing cancer development/progression and to improving health during aging. In this review, we discuss how senescent cells continuously evolve after their initial proliferative arrest and highlight the unifying features that define the senescent state.
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