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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Related Experiment Video

Updated: Aug 2, 2025

Author Spotlight: Mitochondrial Remodeling in Skeletal Muscle
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Enhanced Mitochondria-SR Tethering Triggers Adaptive Cardiac Muscle Remodeling.

Zuzana Nichtová1, Celia Fernandez-Sanz2, Sergio De La Fuente2

  • 1MitoCare, Pathology and Genomic Medicine (Z.N., S.H., D.W., A.B., E.L.S., G.C.), Thomas Jefferson University, Philadelphia, PA.

Circulation Research
|April 14, 2023
PubMed
Summary

Enhancing cardiac mitochondria-sarcoplasmic reticulum (SR) tethering in mice improved heart resilience to stress. This adaptation involved remodeling of cellular structures, preserving energy production and reducing cell death.

Keywords:
ischemiamitochondriamuscle cellsmyocardiumreperfusionsarcoplasmic reticulumtransgenes

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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Function
  • Cellular Physiology

Background:

  • Cardiac function relies on energy from mitochondria and calcium (Ca2+) from the sarcoplasmic reticulum (SR).
  • Mitochondria-SR contacts facilitate excitation-bioenergetics coupling, but pathological stress can lead to overload and cell damage.
  • The role of mitochondria-SR tethers in cardiac health and disease is not fully understood.

Purpose of the Study:

  • To investigate the physiological and pathological relevance of chronically enhancing cardiac mitochondria-SR tethering.
  • To assess how selective, long-term increases in mitochondria-SR contacts affect cardiac function and stress resilience.

Main Methods:

  • A cardiac muscle-specific engineered tether (linker) transgene was introduced into mice.
  • A combination of 2D/3D electron microscopy, biochemical assays, fluorescence imaging, and in vivo/ex vivo cardiac monitoring was employed.
  • Mice expressing the linker were subjected to various stress challenges.

Main Results:

  • The linker increased mitochondria-SR contacts and induced remodeling, forming large mitochondrial clusters.
  • Excitation-bioenergetics coupling was preserved, potentially via enhanced longitudinal contacts and nanotunneling.
  • Mice with enhanced tethering showed reduced vulnerability to beta-adrenergic stress and improved outcomes in ischemia/reperfusion injury, with less myocyte death.

Conclusions:

  • Chronic enhancement of mitochondria-SR contacts, initiated early in life, can lead to adaptive remodeling and a new structural optimum.
  • This remodeling balances enhanced crosstalk with preserved excitation-bioenergetics coupling by increasing the connected mitochondrial pool.
  • Improved Ca2+/reactive oxygen species capacity resulting from this remodeling enhances cardiac resilience to stress-induced by dysregulated Ca2+ signaling.