4.7 Article

Metabolic Stress Mitochondrial Function in Neointimal Formation

Journal

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 39, Issue 6, Pages 991-997

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.118.312196

Keywords

angioplasty; apoptosis; mitochondria; neointima; reactive oxygen species

Funding

  1. National Institutes of Health [R01 HL 108932, F30 HL131078-01, T32 GM007337]
  2. Veterans Affairs Iowa City [I01 BX000163]
  3. American Heart Association [17GRNT33660032]

Ask authors/readers for more resources

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.

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