Mitochondrial function in vascular endothelial cell in diabetes

Meenal Pangare, Ayako Makino

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


Micro- and macrovascular complications are commonly seen in diabetic patients and en-dothelial dysfunction contributes to the development and progression of the complications. Abnormal functions in endothelial cells lead to the increase in vascular tension and atheroscle-rosis, followed by systemic hypertension as well as increased incidence of ischemia and stroke in diabetic patients. Mitochondria are organelles serving as a source of energy production and as regulators of cell survival (e.g., apoptosis and cell development) and ion homeostasis (e.g., H +, Ca 2+). Endothelial mitochondria are mainly responsible for generation of reactive oxy-gen species (ROS) and maintaining the Ca 2+ concentration in the cytosol. There is increasing evidence that mitochondrial morphological and functional changes are implicated in vascular endothelial dysfunction. Enhanced mitochondrial ission and/or attenuated fusion lead to mi-tochondrial fragmentation and disrupt the endothelial physiological function. Abnormal mito-chondrial biogenesis and disturbance of mitochondrial autophagy increase the accumulation of damaged mitochondria, such as irreversibly depolarized or leaky mitochondria, and facilitate cell death. Augmented mitochondrial ROS production and Ca 2+ overload in mitochondria not only cause the maladaptive effect on the endothelial function, but also are potentially detrimen-tal to cell survival. In this article, we review the physiological and pathophysiological role of mitochondria in endothelial function with special focus on diabetes.

Original languageEnglish (US)
Pages (from-to)1-26
Number of pages26
JournalJournal of Smooth Muscle Research
Issue number1
StatePublished - 2012
Externally publishedYes


  • Apoptosis
  • Biogenesis
  • Complications
  • Fission and fusion
  • Mitophagy

ASJC Scopus subject areas

  • Physiology


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