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Updated: Jun 29, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Targeting calcium handling in arrhythmias
Gudrun Antoons1, Karin R Sipido
1Department of Cardiovascular Medicine, Division of Experimental Cardiology, University of Leuven, KUL, Leuven, Belgium.
Abstract:
Abnormal calcium (Ca) handling can contribute to arrhythmogenesis directly by triggering abnormal depolarizations and indirectly by modulating action potential time course and duration. Recent data have shown the importance of these mechanisms in rare genetic diseases but also in more common conditions such as heart failure. Modulating Ca release from the sarcoplasmic reticulum via the ryanodine receptor, Ca uptake via sarcoplasmic reticulum Ca ATPase or Ca removal from the cell via the Na/Ca exchanger, are potential approaches to reduce arrhythmias. New tools allow exploring these ideas. The principles underlying this approach and the first results are critically reviewed.
Insights
Abnormal calcium handling in heart cells can cause arrhythmias. Targeting calcium release, uptake, or removal offers a new strategy for treating heart rhythm disorders like heart failure.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Electrophysiology
Background:
- Abnormal calcium (Ca) handling is a key factor in cardiac arrhythmias, affecting both direct abnormal depolarizations and action potential dynamics.
- These calcium-related mechanisms are implicated in rare genetic disorders and prevalent conditions like heart failure.
Purpose of the Study:
- To review the principles of modulating cellular calcium handling for arrhythmia reduction.
- To discuss the potential of targeting sarcoplasmic reticulum Ca release (ryanodine receptor), Ca uptake (SERCA), and Ca removal (Na/Ca exchanger).
Main Methods:
- Critical review of existing literature and recent data.
- Exploration of novel tools and approaches for studying calcium handling in the heart.
Main Results:
- Dysfunctional calcium handling directly contributes to arrhythmogenesis.
- Modulating key calcium transport proteins (ryanodine receptor, SERCA, Na/Ca exchanger) shows promise in preclinical studies.
- New research tools are enabling deeper investigation into these mechanisms.
Conclusions:
- Targeting cellular calcium handling represents a viable therapeutic strategy for managing cardiac arrhythmias.
- Further research utilizing advanced tools is crucial for translating these findings into clinical practice for heart failure and other conditions.
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Published on: November 3, 2020
11:00Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
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