Science advances · 2026
VMP1 forms a Ca2+ release channel essential for postnatal heartbeat.
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Ma Yuying, Li Qiguang, Jia Yuting, Hao Bo, Li Jiahe, Zhang Ziyi, Yin Na, Fang Sui, Wang Yao, Wu Zhifang, Gao Zhaobing, Xia Bingqing, Peng Min
Аннотация
Normal heart contraction requires synchronized calcium ion (Ca2+) release from the sarcoplasmic reticulum (SR), traditionally attributed to ryanodine receptor 2 (RyR2). Here, we identify vacuole membrane protein 1 (VMP1) as a previously unrecognized SR Ca2+ release channel essential for postnatal cardiac function. VMP1 expression is up-regulated in cardiomyocytes after birth, and its genetic deletion causes severe arrhythmias, dilated cardiomyopathy, and sudden cardiac death. Mechanistically, VMP1 loss results in increased SR Ca2+ content and aberrant cardiac action potentials. Single-channel electrophysiology reveals that VMP1 forms a Ca2+-regulated Ca2+ channel, which senses luminal Ca2+ via aspartic acid 272. Notably, VMP1 expression is elevated in human heart failure, suggesting a pathophysiological role. These findings establish VMP1 as a critical component of the cardiac Ca2+ release machinery and uncover its involvement in heart failure.