Mitochondrial dysfunction in cardiac aging

Biochim Biophys Acta. 2015 Nov;1847(11):1424-33. doi: 10.1016/j.bbabio.2015.07.009. Epub 2015 Jul 17.

Abstract

Cardiovascular diseases are the leading cause of death in most developed nations. While it has received the least public attention, aging is the dominant risk factor for developing cardiovascular diseases, as the prevalence of cardiovascular diseases increases dramatically with increasing age. Cardiac aging is an intrinsic process that results in impaired cardiac function, along with cellular and molecular changes. Mitochondria play a great role in these processes, as cardiac function is an energetically demanding process. In this review, we examine mitochondrial dysfunction in cardiac aging. Recent research has demonstrated that mitochondrial dysfunction can disrupt morphology, signaling pathways, and protein interactions; conversely, mitochondrial homeostasis is maintained by mechanisms that include fission/fusion, autophagy, and unfolded protein responses. Finally, we describe some of the recent findings in mitochondrial targeted treatments to help meet the challenges of mitochondrial dysfunction in aging.

Keywords: Aging; Heart; Mitochondrial dysfunction; Mitostasis.

Publication types

  • Review

MeSH terms

  • Aging / physiology*
  • Animals
  • Autophagy
  • Caloric Restriction
  • Cardiolipins / physiology
  • DNA Damage
  • Energy Metabolism
  • Heart / physiology*
  • Homeostasis
  • Humans
  • Mitochondria / pathology
  • Mitochondria / physiology*
  • Proteins / metabolism
  • Signal Transduction / physiology
  • Unfolded Protein Response

Substances

  • Cardiolipins
  • Proteins