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Cardioprotection during diabetes: the role of mitochondrial DNA

Maria Muravyeva1, Ines Baotic, Martin Bienengraeber

  • 1From the Department of Anesthesiology (M.M., I.B., M.B., Z.J.B., F.S., D.C.W., and J.R.K.), Department of Pharmacology and Toxicology (M.B., D.C.W., and J.R.K.), and Department of Physiology (Z.J.B.), Medical College of Wisconsin, Milwaukee, Wisconsin; and The Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, Wisconsin (J.L.).

Anesthesiology
|December 19, 2013
PubMed
Abstract

Insights

Mitochondrial DNA differences affect how well anesthetic preconditioning protects diabetic rats against heart injury. This study shows mitochondrial genome variations influence reactive oxygen species generation, impacting protection from ischemia-reperfusion injury.

Area of Science:

  • Cardiovascular Science
  • Mitochondrial Biology
  • Anesthesiology

Background:

  • Diabetes mellitus (DM) impairs mitochondrial function and cardioprotective signaling.
  • Mitochondrial DNA (mtDNA) plays a role in DM-induced cardiac dysfunction.
  • Investigating mtDNA's role in anesthetic preconditioning (APC) and ischemia-reperfusion (I/R) injury is crucial.

Purpose of the Study:

  • To determine if mtDNA modulates APC efficacy in diabetic rats.
  • To assess the impact of distinct mitochondrial genomes on cardiac susceptibility to I/R injury.
  • To elucidate the mechanisms underlying APC in diabetic conditions.

Main Methods:

  • Utilized two rat strains with identical nuclear genomes but different mtDNA (T2DN(mtWistar) and T2DN(mtFHH)).
  • Measured myocardial infarct size with and without APC (isoflurane) and N-acetylcysteine (NAC).
  • Assessed mitochondrial redox state, reactive oxygen species (ROS) generation, and mitochondrial permeability transition pore (MPTP) opening in cardiomyocytes.

Main Results:

  • APC reduced infarct size in Wistar and T2DN(mtWistar) rats but not in T2DN(mtFHH) rats.
  • NAC restored APC in T2DN(mtFHH) rats and abolished protection in control rats.
  • APC delayed MPTP opening in T2DN(mtWistar) but not T2DN(mtFHH) cardiomyocytes; isoflurane increased ROS production, most notably in T2DN(mtFHH) cardiomyocytes.

Conclusions:

  • Mitochondrial genome variations significantly influence the susceptibility of diabetic hearts to I/R injury.
  • mtDNA modulates isoflurane-induced ROS generation, thereby affecting APC efficacy.
  • Targeting mtDNA-related pathways may offer novel therapeutic strategies for cardioprotection in diabetic patients.

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