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Related Experiment Video

Updated: Jun 16, 2026

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
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Targeting Mitochondrial Dysfunction With Elamipretide (SS-31) Improves Skeletal Muscle Performance in a HFpEF Rat

Beatrice Vahle1, Sven Weidner2, André Tomalka2

  • 1Heart Center Dresden, Laboratory of Molecular and Experimental Cardiology, TU Dresden, Germany (B.V., A.S., A.A., A.M., P.B., J.F., A.L., V.A.).

Circulation. Heart Failure
|June 15, 2026
PubMed
Summary

Elamipretide treatment improved skeletal muscle function in heart failure with preserved ejection fraction (HFpEF) rats by stabilizing cardiolipin and enhancing mitochondrial respiration. This suggests Elamipretide as a potential therapy for HFpEF-related exercise intolerance.

Keywords:
animalsheart failuremitochondriaobesitystroke volume

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A Murine Model of Hyperlipidemia-Induced Heart Failure with Preserved Ejection Fraction
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A Murine Model of Hyperlipidemia-Induced Heart Failure with Preserved Ejection Fraction

Published on: March 29, 2024

Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Skeletal Muscle Physiology

Background:

  • Exercise intolerance in heart failure with preserved ejection fraction (HFpEF) is linked to skeletal muscle and mitochondrial dysfunction.
  • Altered cardiolipin integrity in HFpEF myocardium suggests cardiolipin stabilizers like Elamipretide as potential therapeutics.

Purpose of the Study:

  • To investigate cardiolipin dysregulation in the skeletal muscle of HFpEF rats.
  • To evaluate the therapeutic effect of Elamipretide on skeletal muscle dysfunction in HFpEF.

Main Methods:

  • Utilized Zucker fatty spontaneously hypertensive heart failure F1 hybrid obese rats (HFpEF model) and lean controls.
  • Administered Elamipretide or NaCl to HFpEF rats for 12 weeks.
  • Assessed skeletal muscle function, mitochondrial respiration, histology, and molecular markers.

Main Results:

  • HFpEF rats showed reduced cardiolipin levels, contractile dysfunction, titin hyperphosphorylation, fiber atrophy, and increased oxidative stress.
  • Elamipretide treatment significantly improved whole muscle and single-fiber contractile function.
  • Elamipretide reversed titin hyperphosphorylation, prevented atrophy, and potentially improved mitochondrial function.

Conclusions:

  • Cardiolipin stabilization is crucial for maintaining mitochondrial and contractile function in HFpEF skeletal muscle.
  • Elamipretide demonstrates potential as a therapeutic agent for skeletal muscle dysfunction in HFpEF.