Cardiomyocytes proliferate during fetal life but lose their ability to proliferate soon after birth
and further increases in cardiac mass are achieved through an increase in cell size or
hypertrophy. Mammalian target of rapamycin complex 1 (mTORC1) is critical for cell growth
and proliferation. Rheb (Ras homologue enriched in brain) is one of the most important
upstream regulators of mTORC1. Here, we attempted to clarify the role of Rheb in the heart
using cardiac-specific Rheb-deficient mice (Rheb−/−). Rheb−/− mice died from postnatal day …