Novel contributors and mechanisms of cellular senescence in hypertension-associated premature vascular aging

Cameron G. McCarthy, Camilla F. Wenceslau, R. Clinton Webb, Bina Joe

Research output: Contribution to journalReview article

Abstract

Hypertension has been described as a condition of premature vascular aging, relative to actual chronological age. In fact, many factors that contribute to the deterioration of vascular function as we age are accelerated in hypertension. Nonetheless, the precise mechanisms that underlie the aged phenotype of arteries from hypertensive patients and animals remain elusive. Cellular senescence is an age-related physiologic process in which cells undergo irreversible growth arrest. Although controlled senescence negatively regulates cell proliferation and promotes tissue regeneration, uncontrolled senescence can contribute to disease pathogenesis by presenting the senescence-associated secretory phenotype, in which molecules such as proinflammatory cytokines, matrix metalloproteases, and reactive oxygen species are released into tissue microenvironments. This review will address and critically evaluate the current literature on the role of cellular senescence in hypertension, with particular emphasis on cells types that mediate and modulate vascular function and structure.

Original languageEnglish (US)
Pages (from-to)709-719
Number of pages11
JournalAmerican journal of hypertension
Volume32
Issue number8
DOIs
StatePublished - Jan 1 2019

Fingerprint

Premature Aging
Cell Aging
Blood Vessels
Hypertension
Phenotype
Metalloproteases
Regeneration
Reactive Oxygen Species
Arteries
Cell Proliferation
Cytokines
Growth

Keywords

  • Blood pressure
  • Cellular senescence
  • Hypertension
  • Vascular aging

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Novel contributors and mechanisms of cellular senescence in hypertension-associated premature vascular aging. / McCarthy, Cameron G.; Wenceslau, Camilla F.; Webb, R. Clinton; Joe, Bina.

In: American journal of hypertension, Vol. 32, No. 8, 01.01.2019, p. 709-719.

Research output: Contribution to journalReview article

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