Cardiac aging: from molecular mechanisms to significance in human health and disease

Dao-Fu Dai, Tony Chen, Simon C Johnson, Hazel Szeto, Peter S Rabinovitch

Research output: Contribution to journalReview articlepeer-review

247 Citations (Scopus)

Abstract

Cardiovascular diseases (CVDs) are the major causes of death in the western world. The incidence of cardiovascular disease as well as the rate of cardiovascular mortality and morbidity increase exponentially in the elderly population, suggesting that age per se is a major risk factor of CVDs. The physiologic changes of human cardiac aging mainly include left ventricular hypertrophy, diastolic dysfunction, valvular degeneration, increased cardiac fibrosis, increased prevalence of atrial fibrillation, and decreased maximal exercise capacity. Many of these changes are closely recapitulated in animal models commonly used in an aging study, including rodents, flies, and monkeys. The application of genetically modified aged mice has provided direct evidence of several critical molecular mechanisms involved in cardiac aging, such as mitochondrial oxidative stress, insulin/insulin-like growth factor/PI3K pathway, adrenergic and renin angiotensin II signaling, and nutrient signaling pathways. This article also reviews the central role of mitochondrial oxidative stress in CVDs and the plausible mechanisms underlying the progression toward heart failure in the susceptible aging hearts. Finally, the understanding of the molecular mechanisms of cardiac aging may support the potential clinical application of several "anti-aging" strategies that treat CVDs and improve healthy cardiac aging.

Original languageEnglish
Pages (from-to)1492-526
Number of pages35
JournalAntioxidants and Redox Signaling
Volume16
Issue number12
DOIs
Publication statusPublished - 15 Jun 2012

Keywords

  • Animals
  • Cardiovascular Diseases/metabolism
  • Humans
  • Mitochondria/metabolism
  • Oxidative Stress/physiology
  • Signal Transduction/physiology

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