Aug 6, 2018

Cellular senescence: Molecular mechanisms and pathogenicity

Journal of Cellular Physiology
Wenqiang Wei, Shaoping Ji

Abstract

Cellular senescence is the arrest of normal cell division. Oncogenic genes and oxidative stress, which cause genomic DNA damage and generation of reactive oxygen species, lead to cellular senescence. The senescence-associated secretory phenotype is a distinct feature of senescence. Senescence is normally involved in the embryonic development. Senescent cells can communicate with immune cells to invoke an immune response. Senescence emerges during the aging process in several tissues and organs. In fact, increasing evidence shows that cellular senescence is implicated in aging-related diseases, such as nonalcoholic fatty liver disease, obesity and diabetes, pulmonary hypertension, and tumorigenesis. Cellular senescence can also be induced by microbial infection. During cellular senescence, several signaling pathways, including those of p53, nuclear factor-κB (NF-κB), mammalian target of rapamycin, and transforming growth factor-beta, play important roles. Accumulation of senescent cells can trigger chronic inflammation, which may contribute to the pathological changes in the elderly. Given the variety of deleterious effects caused by cellular senescence in humans, strategies have been proposed to control senescence. In this revi...Continue Reading

  • References143
  • Citations12

Mentioned in this Paper

Embryo
Study
Immune Response
Biochemical Pathway
Transforming Growth Factor beta
Cell Aging
Immune Effector Cell
Cell Division
Molecular_function
FRAP1 protein, human

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