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Ryanodine receptor dysfunction in human disorders.

Alexander Kushnir1, Benjamin Wajsberg2, Andrew R Marks2

  • 1Department of Physiology and Cellular Biophysics, Clyde and Helen Wu Center for Molecular Cardiology, Columbia University Vagelos College of Physicians and Surgeons, New York, NY 10032, USA; Department of Medicine, Division of Cardiology, Columbia University Vagelos College of Physicians and Surgeons, New York, NY 10032, USA.

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|July 25, 2018
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Summary
This summary is machine-generated.

Intracellular calcium (Ca2+) regulation by the ryanodine receptor (RyR) is vital for cell function. RyR dysfunction contributes to various diseases, prompting the development of targeted therapies.

Keywords:
Alzheimer's diseaseArrhythmiasCPVTDiabetesDuchenne muscular dystrophyHeart failurePTSDSarcopeniaSudden cardiac death

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Physiology

Background:

  • Intracellular calcium (Ca2+) homeostasis is essential for cellular functions.
  • The ryanodine receptor (RyR) on the sarco/endoplasmic reticulum (SR/ER) controls Ca2+ release.
  • RyR dysfunction is linked to numerous inherited and non-inherited diseases.

Purpose of the Study:

  • To review the link between human disorders and ryanodine receptor (RyR) dysfunction.
  • To explore novel therapeutic strategies targeting RyR.

Main Methods:

  • Literature review of studies on RyR and human diseases.
  • Analysis of evidence linking RyR dysfunction to specific pathologies.
  • Identification and description of emerging RyR-targeted therapeutic approaches.

Main Results:

  • RyR-mediated Ca2+ handling is critical for muscle contraction and neurotransmission.
  • Dysfunctional RyR is implicated in heart failure, arrhythmias, myopathies, diabetes, and neurodegeneration.
  • Novel therapeutic strategies aim to correct RyR function.

Conclusions:

  • Ryanodine receptor (RyR) dysfunction is a significant factor in various human diseases.
  • Targeting RyR offers promising therapeutic avenues for treating these conditions.