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Updated: Apr 22, 2026

Generation and Expansion of Human Cardiomyocytes from Patient Peripheral Blood Mononuclear Cells
Published on: February 12, 2021
Alpha-catenins control cardiomyocyte proliferation by regulating Yap activity
Jifen Li1, Erhe Gao1, Alexia Vite1
1From the Department of Medicine, Center for Translational Medicine, Thomas Jefferson University, Philadelphia, PA (J.L., E.G., A.V., R.Y., L.G., G.L.R.); Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium (S.G., F.v.R.); Inflammation Research Center, Flanders Institute for Biotechnology (VIB), Ghent, Belgium (S.G., F.v.R.); and INSERM UMR-1060, Laboratoire CarMeN, Université Lyon 1, Faculté de médecine, Rockefeller et Charles Merieux Lyon-Sud, Lyon, France (L.G.). Current address for E.G.: Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA.
Inhibiting α-catenins promotes heart regeneration by increasing cardiomyocyte proliferation via Yap activation. This finding offers a new strategy for treating cardiac injury and improving heart function after myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Regenerative Medicine
Background:
- Mammalian heart muscle cells lose division ability post-birth, hindering repair of injured hearts.
- The transcriptional coactivator Yes-associated protein (Yap) is key for cardiomyocyte proliferation, but its regulators are unclear.
Purpose of the Study:
- To investigate the role of α-catenins in cardiac function.
- To explore α-catenins as regulators of Yap in the heart.
Main Methods:
- Generated cardiac-specific αE- and αT-catenin double knockout mice (perinatal and inducible adult).
- Assessed cardiomyocyte proliferation, Yap activity, and cardiac gene expression.
- Utilized neonatal rat cardiomyocyte knockdown models.
Main Results:
- Perinatal α-catenin depletion increased cardiomyocyte numbers and Yap activity.
- Adult α-catenin inactivation improved contractility post-myocardial infarction.
- Knockdown of α-catenins in neonatal cardiomyocytes increased proliferation, dependent on Yap.
Conclusions:
- α-catenins critically regulate Yap, essential for cardiomyocyte proliferation.
- Inhibiting α-catenins is a potential strategy for myocardial regeneration after injury.
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