Mitochondria and Cardiac Hypertrophy

Adv Exp Med Biol. 2017:982:203-226. doi: 10.1007/978-3-319-55330-6_11.

Abstract

Cardiac tissue responds to long-term hemodynamic load through initiation of a hypertrophic remodeling program. Importantly, if not counteracted this response will eventually lead to organ failure. Cardiac hypertrophic adaptations are complex, and involve multiple cellular events and the mechanisms underlying the development of cardiac hypertrophy are not well understood. Mitochondrial dysfunction has been indicated as a potential and important player in the development of cardiac hypertrophy. Additionally, substantial evidence shows that a significant portion of mitochondrial processes, necessary for normal cardiomyocyte physiology, are impacted by these hypertrophic changes. In this chapter, we will present and discuss the adaptations and changes in the mitochondrial electron transport system, mitochondrial metabolism, mitochondrial biogenesis, oxidative stress, the opening of the mitochondrial permeability transition pore following hypertrophic stimuli, as well as, review the various drugs (targeting mitochondria) that can be used in treatment of cardiac hypertrophy.

Keywords: Antioxidants; Eletron Transport Chain; Hypertrophy; Mitochondria; Oxidation; Oxidative stress.

Publication types

  • Review

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Calcium Signaling*
  • Cardiomegaly / metabolism*
  • Cardiomegaly / pathology
  • Cardiomegaly / physiopathology
  • Energy Metabolism*
  • Humans
  • Mitochondria, Heart / metabolism*
  • Mitochondria, Heart / pathology
  • Mitochondrial Dynamics
  • Mitochondrial Membrane Transport Proteins / metabolism
  • Mitochondrial Permeability Transition Pore
  • Myocytes, Cardiac / metabolism*
  • Myocytes, Cardiac / pathology
  • Organelle Biogenesis
  • Oxidative Stress

Substances

  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Permeability Transition Pore
  • Calcium