Related Experiment Video
Updated: Jan 16, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Targeting Calcium Regulation for Heart Failure and Arrhythmia Therapeutics: A Critical Review
Gabriel Redel-Traub1, Steven O Marx1,2,3,4, Andrew R Marks2,4
1Department of Medicine (G.R.-T., S.O.M.), Columbia University, New York, NY.
Insights
Defective calcium (Ca2+) handling in heart cells drives heart failure and arrhythmias. Targeting Ca2+-handling proteins offers a promising therapeutic strategy for these conditions.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Heart failure (HF) and cardiac arrhythmias are major global health issues.
- Defective calcium (Ca2+) handling in cardiac myocytes is a key mechanism in HF and arrhythmias.
- Current therapies have limitations, necessitating novel strategies.
Purpose of the Study:
- To review the role of Ca2+-handling proteins in heart failure and arrhythmias.
- To examine recent discoveries and challenges in targeting these proteins.
- To highlight therapeutic implications for developing new treatments.
Main Methods:
- Critical assessment of current research on Ca2+-handling proteins.
- Examination of paradigm-shifting discoveries and clinical trial outcomes.
- Analysis of protein expression and function in health and disease.
Main Results:
- Ca2+ handling defects are central to the pathogenesis of HF and arrhythmias.
- Targeting Ca2+-handling proteins presents significant therapeutic potential.
- Understanding protein function is key to developing effective treatments.
Conclusions:
- Improved understanding of Ca2+-handling proteins is crucial for novel therapeutics.
- Targeted therapies could fundamentally alter the course of heart failure and arrhythmias.
- Further research is needed to translate discoveries into clinical practice.
Abstract:
Despite advances in pharmacologic and procedural therapies, heart failure (HF) and cardiac arrhythmias remain significant global health burdens, highlighting the urgent need for novel therapeutic strategies. Defective Ca2+ handling in cardiac myocytes is recognized as a central pathogenic mechanism underlying both heart failure and atrial and ventricular arrhythmias. In this review, we critically assess the current state of research on Ca2+-handling proteins and their role in causing heart failure and arrhythmias, highlighting therapeutic implications. Recent paradigm-shifting discoveries, clinical trial outcomes, and challenges of targeting Ca2+-handling proteins are examined. As outlined in this review, an improved understanding of the relevant proteins and their differential expression and function in human health and disease is crucial for developing Ca2+ handling-targeted therapeutics that can fundamentally alter the natural history of heart failure and arrhythmias.
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