AI Article Synopsis

  • Cellular senescence is a stable state of cell-cycle arrest that influences processes like aging, cancer development, and embryonic growth.
  • The study examines the role of mitochondria in senescent cells, finding that these cells have increased reactive oxygen species (ROS) levels and heightened glucose metabolism, along with significant mitochondrial changes.
  • Ultimately, dysfunctional mitochondria lead to a decline in membrane potential and trigger apoptosis, suggesting that mitochondrial activity is crucial for determining the fate of senescent cells.

Article Abstract

Defined as stable cell-cycle arrest, cellular senescence plays an important role in diverse biological processes including tumorigenesis, organismal aging, and embryonic development. Although increasing evidence has documented the metabolic changes in senescent cells, mitochondrial function and its potential contribution to the fate of senescent cells remain largely unknown. Here, using two in vitro models of cellular senescence induced by doxorubicin treatment and prolonged passaging of neonatal human foreskin fibroblasts, we report that senescent cells exhibited high ROS level and augmented glucose metabolic rate concomitant with both morphological and quantitative changes of mitochondria. Furthermore, mitochondrial membrane potential depolarized at late stage of senescent cells which eventually led to apoptosis. Our study reveals that mitochondrial hyper-function contributes to the implementation of cellular senescence and we propose a model in which the mitochondrion acts as the key player in promoting fate-determination in senescent cells.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053727PMC
http://dx.doi.org/10.18632/oncotarget.8536DOI Listing

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