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RyR2 and Calcium Release in Heart Failure.

Jean-Pierre Benitah1, Romain Perrier1, Jean-Jacques Mercadier1

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Summary

Heart failure (HF) involves impaired Ca2+ handling, particularly in the sarcoplasmic reticulum (SR) Ca2+ release channel (RyR2). Modifications to RyR2 contribute to reduced heart function and arrhythmias in HF.

Keywords:
atrial fibrillationcalciumexcitation contraction couplingheart failureryanodine receptorsinus node

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Heart failure (HF) is characterized by the heart's inability to meet the body's circulatory demands.
  • Dysfunctional calcium (Ca2+) handling is a key contributor to impaired cardiac contraction and relaxation in HF.
  • The sarcoplasmic reticulum (SR) Ca2+ release channel, type 2 ryanodine receptor (RyR2), plays a critical role in cardiac Ca2+ cycling.

Purpose of the Study:

  • This review focuses on alterations in RyR2 function and its contribution to the pathophysiology of heart failure.
  • To explore the impact of RyR2 modifications on cardiac contractility and arrhythmogenesis in HF.
  • To discuss recent findings in both HF with reduced and preserved ejection fraction.

Main Methods:

  • Literature review of experimental and clinical studies on RyR2 in heart failure models.
  • Analysis of research investigating RyR2 phosphorylation, oxidation, and protein interactions.
  • Examination of studies on structural remodeling affecting RyR2 function.

Main Results:

  • HF is associated with reduced RyR2 responsiveness to L-type calcium channel activation due to cardiomyocyte remodeling.
  • Enhanced RyR2 phosphorylation (e.g., at S2814) and oxidation are observed in human and experimental HF.
  • Diminished FKBP12.6 expression and altered RyR2 function may contribute to contractile dysfunction and arrhythmias.

Conclusions:

  • Alterations in RyR2 are central to the diminished cardiac function seen in heart failure.
  • Modified RyR2 function contributes to both reduced contractility and increased susceptibility to arrhythmias in HF.
  • RyR2 dysfunction may also underlie supraventricular defects, including sinus node dysfunction and atrial fibrillation, in HF patients.