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.
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.
More Related Videos
11:00Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
09:26Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart
Published on: September 10, 2015
Related Concept Videos
Heart Failure Drugs: Inotropic Agents
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Heart Failure V: Medical Management
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...