Time-dependent replicative senescence vs. disturbed flow-induced pre-mature aging in atherosclerosis

Abishai Dominic, Priyanka Banerjee, Dale J. Hamilton, Nhat-Tu Le, Jun ichi Abe

Research output: Contribution to journalReview article

Abstract

Accumulation of senescent cells has a causative role in the pathology of age-related disorders including atherosclerosis (AS) and cardiovascular diseases (CVDs). However, the concept of senescence is now drastically changing, and the new concept of senescence-associated reprogramming/stemness has emerged, suggesting that senescence is not merely related to “cell cycle arrest” or halting various cellular functions. It is well known that disturbed flow (D-flow) accelerates pre-mature aging and plays a significant role in the development of AS. We will discuss in this review that pre-mature aging induced by D-flow is not comparable to time-dependent aging, particularly with a focus on the possible involvement of senescence-associated secretory phenotype (SASP) in senescence-associated reprogramming/stemness, or increasing cell numbers. We will also present our outlook of nicotinamide adenine dinucleotides (NAD)+ deficiency-induced mitochondrial reactive oxygen species (mtROS) in evoking SASP by activating DNA damage response (DDR). MtROS plays a key role in developing cross-talk between nuclear-mitochondria, SASP, and ultimately atherosclerosis formation. Although senescence induced by time and various stress factors is a classical concept, we wish that the readers will see the undergoing Copernican-like change in this concept, as well as to recognize the significant contrast between pre-mature aging induced by D-flow and time-dependent aging.

Original languageEnglish (US)
Article number101614
JournalRedox Biology
DOIs
StatePublished - Jan 1 2020

Keywords

  • Aging
  • Atherosclerosis
  • Oxidative stress
  • Senescence
  • Senescent-associated stemness
  • Telomere shortening

ASJC Scopus subject areas

  • Organic Chemistry
  • Clinical Biochemistry

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