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Updated: Feb 12, 2026
07:48
Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration
Published on: May 24, 2016
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LARP7 promotes postnatal cardiac regeneration by facilitating G2/M phase transition
Shasha Zhang1, Kang Cheng1, Junhao Xiong1
1Key Laboratory of Systems Biomedicine, Shanghai Center for Systems Biomedicine, Department of Cardiovascular Surgery, Shanghai Chest Hospital, Engineering Research Center of Techniques and Instruments for Diagnosis and Treatment of Congenital Heart Disease, Institute of Developmental and Regenerative Medicine, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Journal of Molecular and Cellular Cardiology
|February 10, 2026
Summary
Scientists identified La Ribonucleoprotein 7 (LARP7) as a key factor in heart regeneration. Overexpressing LARP7 promotes cardiomyocyte proliferation and enhances cardiac repair after injury, offering a new therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Regenerative Medicine
Background:
- Adult mammalian cardiomyocyte regeneration is limited, hindering heart repair post-injury.
- La Ribonucleoprotein 7 (LARP7) regulates transcription and DNA damage response, but its role in cardiac regeneration is unknown.
Purpose of the Study:
- To investigate the role of LARP7 in cardiomyocyte proliferation and heart regeneration.
- To elucidate the molecular mechanisms by which LARP7 influences cardiac repair.
Main Methods:
- Assessed LARP7 expression correlation with myocardial regeneration.
- Overexpressed LARP7 in cardiomyocytes to evaluate its effect on proliferation and regenerative window.
- Investigated the SIRT1/p53 pathway and its interaction with LARP7, p21, CDK1/CCNB.
- Utilized a dual AAV9 system for co-expression of LARP7, CCND1, and CDK4.
Main Results:
- LARP7 expression positively correlates with myocardial regeneration.
- LARP7 overexpression moderately promotes cardiomyocyte proliferation and extends the neonatal heart's regenerative window.
- LARP7 suppresses p21 via the SIRT1/p53 pathway, enhancing G2/M phase transition and CDK1/CCNB activity.
- Co-expression of LARP7 with CCND1 and CDK4 via AAV9 significantly boosts cardiac regeneration and recovery.
Conclusions:
- LARP7 acts as a novel molecular switch for cell cycle regulation in cardiomyocytes.
- Ectopic expression of LARP7, particularly with G1/S regulators, enhances cardiac regeneration.
- LARP7 presents a promising therapeutic target for improving cardiac repair after damage.
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