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VMP1 forms a Ca2+ release channel essential for postnatal heartbeat
Yuying Ma1,2,3, Qiguang Li4,5, Yuting Jia2,6,7
1State Key Laboratory of Molecular Oncology, Institute for Immunology, Beijing Key Laboratory of Immunological Research of Allergy, School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing, China.
Science Advances
|June 12, 2026
Summary
Vacuole membrane protein 1 (VMP1) is a newly discovered calcium channel crucial for heart function. Its absence causes fatal heart conditions, highlighting its role in cardiac health and heart failure.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Normal heart contraction depends on synchronized calcium ion (Ca2+) release from the sarcoplasmic reticulum (SR).
- Ryanodine receptor 2 (RyR2) has been traditionally considered the primary SR Ca2+ release channel.
Purpose of the Study:
- To identify novel SR Ca2+ release channels involved in cardiac function.
- To investigate the role of vacuole membrane protein 1 (VMP1) in the heart.
Main Methods:
- Genetic deletion of VMP1 in cardiomyocytes.
- Analysis of cardiac function, arrhythmias, and action potentials.
- Single-channel electrophysiology to characterize VMP1 channel activity.
Main Results:
- VMP1 expression increases postnatally in cardiomyocytes.
- VMP1 genetic deletion leads to severe arrhythmias, dilated cardiomyopathy, and sudden cardiac death.
- VMP1 deficiency causes increased SR Ca2+ content and abnormal cardiac action potentials.
- VMP1 functions as a Ca2+-regulated channel sensing luminal Ca2+.
Conclusions:
- VMP1 is a critical, previously unrecognized SR Ca2+ release channel essential for postnatal cardiac function.
- Elevated VMP1 expression in human heart failure suggests a pathophysiological role.
- VMP1 is a key component of cardiac Ca2+ release and is implicated in heart failure.
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