VMP1 forms a Ca(2+) release channel essential for postnatal heartbeat.
Y, M., Q, L., Y, J., B, H., J, L., Z, Z., N, Y., S, F., Y, W., & Z, W. (2026). VMP1 forms a Ca(2+) release channel essential for postnatal heartbeat.. Science advances. https://doi.org/10.1126/sciadv.adz0706
Y M, Q L, Y J, B H, J L, Z Z, et al. VMP1 forms a Ca(2+) release channel essential for postnatal heartbeat.. Science advances. 2026; doi: 10.1126/sciadv.adz0706
Y M, Q L, Y J, et al. VMP1 forms a Ca(2+) release channel essential for postnatal heartbeat.[J]. Science advances. 2026. DOI: 10.1126/sciadv.adz0706.
@article{y2026,
author = {Ma Y and Li Q and Jia Y and Hao B and Li J and Zhang Z and Yin N and Fang S and Wang Y and Wu Z},
title = {VMP1 forms a Ca(2+) release channel essential for postnatal heartbeat.},
journal = {Science advances},
year = {2026},
doi = {10.1126/sciadv.adz0706},
note = {PMID: 42284404},
}
TY - JOUR AU - Ma Y AU - Li Q AU - Jia Y AU - Hao B AU - Li J AU - Zhang Z AU - Yin N AU - Fang S AU - Wang Y AU - Wu Z TI - VMP1 forms a Ca(2+) release channel essential for postnatal heartbeat. T2 - Science advances PY - 2026 DO - 10.1126/sciadv.adz0706 AN - PMID:42284404 ER -
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.