Authors
Honghai Liu, Niyatie Ammanamanchi, Jocelyn D Mich-Basso, Brian K Panama, Yao Li, Winston Huang, Dena Almeida, Christopher M Lewarchik, Brendan Lo, Yijen Wu, Michael Gotthardt, Michael I Kotlikoff, Wolfgang Baehr, Randall Rasmusson, Guy Salama, Bernhard Kühn
Published in
The Journal of cell biology. Volume 225. Issue 8. Aug 03, 2026. Epub Jun 25, 2026.
Abstract
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.
PMID:
42347846
Bibliographic data and abstract were imported from PubMed on 25 Jun 2026.
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