Mitophagy and heart failure

J Mol Med (Berl). 2015 Mar;93(3):253-62. doi: 10.1007/s00109-015-1254-6. Epub 2015 Jan 23.

Abstract

Cardiac mitochondria are responsible for generating energy in the form of ATP through oxidative phosphorylation and are crucial for cardiac function. Mitochondrial dysfunction is a major contributor to loss of myocytes and development of heart failure. Myocytes have quality control mechanisms in place to ensure a network of functional mitochondria. Damaged mitochondria are degraded by a process called mitochondrial autophagy, or mitophagy, where the organelle is engulfed by an autophagosome and subsequently delivered to a lysosome for degradation. Evidence suggests that mitophagy is important for cellular homeostasis, and reduced mitophagy leads to inadequate removal of dysfunctional mitochondria. In this review, we discuss the regulation of mitophagy and the emerging evidence of the cardioprotective role of mitophagy. We also address the prospect of therapeutically targeting mitophagy to treat patients with cardiovascular disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium Signaling
  • Cardiotonic Agents / pharmacology
  • Cardiotonic Agents / therapeutic use
  • Heart Failure / drug therapy
  • Heart Failure / metabolism
  • Heart Failure / pathology*
  • Humans
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / metabolism
  • Mitophagy*

Substances

  • Cardiotonic Agents