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Mitochondrial Metabolism in Aging Heart.

Edward J Lesnefsky1, Qun Chen1, Charles L Hoppel2

  • 1From the Division of Cardiology, Department of Medicine, Pauley Heart Center (E.J.L, Q.C.), Departments of Biochemistry and Molecular Biology and Physiology and Biophsyics (E.J.L.), Virginia Commonwealth University, Richmond, VA (E.J.L., Q.C.); Medical Service, McGuire Veterans Affairs Medical Center, Richmond, VA (E.J.L.); and Departments of Pharmacology (C.L.H.) and Medicine (E.J.L., C.L.H.), Center for Mitochondrial Disease (C.L.H.), Case Western Reserve University, School of Medicine, Cleveland, OH.

Circulation Research
|May 14, 2016
PubMed
Summary

Aging impairs heart mitochondria function, reducing fatty acid oxidation and increasing glucose reliance. These mitochondrial defects enhance oxidative stress and cell death, offering new therapeutic targets for age-related cardiac conditions.

Keywords:
cardiolipinelectron transport chain complex proteinsfatty acid oxidation complexoxidative phosphorylationreactive oxygen species

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Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Gerontology

Background:

  • The aged heart displays heightened sensitivity to stress, linked to altered mitochondrial metabolism.
  • Key features include impaired metabolic flexibility, reduced fatty acid oxidation, and increased glucose dependence.

Purpose of the Study:

  • To investigate the impact of aging on cardiac mitochondrial function and identify potential therapeutic targets.
  • To elucidate the mechanisms behind age-related cardiac dysfunction at the mitochondrial level.

Main Methods:

  • Analysis of mitochondrial oxidative phosphorylation in aged versus young hearts.
  • Assessment of specific mitochondrial complexes (III and IV) activity.
  • Evaluation of mitochondrial content and function in interfibrillar regions.

Main Results:

  • Aging significantly impairs mitochondrial oxidative phosphorylation, particularly in interfibrillar mitochondria.
  • Activity of complexes III and IV decreases, leading to reduced respiration.
  • Mitochondrial content diminishes, resulting in a ~50% functional deficit affecting all substrates.

Conclusions:

  • Defective mitochondria in aged hearts contribute to increased oxidant production, oxidative injury, and cell death signaling.
  • Targeting mitochondrial defects (proteome, electron transport, biogenesis, mitophagy, fission/fusion) offers novel therapeutic strategies for age-related cardiac disease.
  • Preemptive treatment of age-related mitochondrial dysfunction may prevent disease-induced cardiac dysfunction.