Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.
H, L., N, A., JD, M.B., BK, P., Y, L., W, H., D, A., CM, L., B, L., & Y, W. (2026). Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.. The Journal of cell biology. https://doi.org/10.1083/jcb.202505134
H L, N A, JD MB, BK P, Y L, W H, et al. Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.. The Journal of cell biology. 2026; doi: 10.1083/jcb.202505134
H L, N A, JD MB, et al. Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.[J]. The Journal of cell biology. 2026. DOI: 10.1083/jcb.202505134.
@article{h2026,
author = {Liu H and Ammanamanchi N and Mich-Basso JD and Panama BK and Li Y and Huang W and Almeida D and Lewarchik CM and Lo B and Wu Y},
title = {Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation.},
journal = {The Journal of cell biology},
year = {2026},
doi = {10.1083/jcb.202505134},
note = {PMID: 42347846},
}
TY - JOUR AU - Liu H AU - Ammanamanchi N AU - Mich-Basso JD AU - Panama BK AU - Li Y AU - Huang W AU - Almeida D AU - Lewarchik CM AU - Lo B AU - Wu Y TI - Sequential changes in calcium transients during M phase regulate cardiomyocyte proliferation. T2 - The Journal of cell biology PY - 2026 DO - 10.1083/jcb.202505134 AN - PMID:42347846 ER -
Heart muscle growth and regeneration require the proliferation of cardiomyocytes. Rapid pulsatile increases in cytosolic Ca2+ concentration, called calcium transients (CaTs), trigger cardiomyocyte contractions, but how cardiomyocytes adapt Ca2+ signaling during proliferation is largely unknown. Here, we show that cardiomyocyte proliferation requires changes in Ca2+ signaling. Cardiomyocytes undergo a sequence of CaT changes during M phase: CaT amplitudes begin to decline in prometaphase, reach a minimum in metaphase, rise during anaphase, and return to the original state in daughter cardiomyocytes. Spindle poles show decreased Ca2+ levels during prometaphase and metaphase. Localized reduction of Ca2+ levels at spindle poles is mediated by dynein 1-dependent SERCA2a accumulation. Active cyclin-dependent kinase 1 (CDK1) induces both the decrease in CaT amplitudes and the accumulation of SERCA2a at the spindle poles, whereas CDK1 inhibition reverses these effects. Forcing an increase in cytosolic Ca2+ levels by blocking SERCA2a during prometaphase and metaphase disrupts mitosis and produces binucleated cardiomyocytes, underscoring the essential role of Ca2+ signaling changes for cardiomyocyte proliferation.