Metabolic Stress

Arterioscler Thromb Vasc Biol. 2019 Jun;39(6):991-997. doi: 10.1161/ATVBAHA.118.312196.

Abstract

Mitochondria regulate major aspects of cell function by producing ATP, contributing to Ca2+ signaling, influencing redox potential, and controlling levels of reactive oxygen species. In this review, we will discuss recent findings that illustrate how mitochondrial respiration, Ca2+ handling, and production of reactive oxygen species affect vascular smooth muscle cell function during neointima formation. We will review mitochondrial fission/fusion as fundamental mechanisms for smooth muscle proliferation, migration, and metabolism and examine the role of mitochondrial mobility in cell migration. In addition, we will summarize novel aspects by which mitochondria regulate apoptosis.

Keywords: angioplasty; apoptosis; mitochondria; neointima; reactive oxygen species.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Cell Movement / genetics
  • Cell Proliferation
  • Cells, Cultured
  • Humans
  • Mitochondria / metabolism*
  • Mitochondrial Dynamics / genetics
  • Muscle, Smooth, Vascular / metabolism*
  • Neointima / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Signal Transduction / genetics
  • Stress, Physiological / genetics*
  • bcl-2 Homologous Antagonist-Killer Protein / genetics*

Substances

  • BAK1 protein, human
  • Reactive Oxygen Species
  • bcl-2 Homologous Antagonist-Killer Protein