Research progress on myocardial regeneration: what is new?

The regeneration capacity of cardiomyocytes (CMs) is retained in neonatal mouse hearts but is limited in adult mouse hearts. Myocardial infarction (MI) in adult hearts usually leads to the loss of large amounts of cardiac tissue, and then accelerates the process of cardiac remodeling and heart failu...

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Bibliographic Details
Published in:Chinese medical journal 2020-03, Vol.133 (6), p.716-723
Main Authors: Du, Chong, Fan, Yi, Li, Ya-Fei, Wei, Tian-Wen, Wang, Lian-Sheng
Format: Article
Language:English
Subjects:
Animals
Cardiac function
Cardiomyocytes
Cardiovascular disease
Cell cycle
Cell Proliferation - genetics
Cell Proliferation - physiology
Deoxyribonucleic acid
DNA
Fibroblasts
Gene expression
Humans
Kinases
Mammals
MicroRNAs
Myocardial Infarction - metabolism
Myocardial Infarction - pathology
Myocardium - metabolism
Myocardium - pathology
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
Review
Rodents
Signal Transduction - genetics
Signal Transduction - physiology
Transcription factors
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Summary:The regeneration capacity of cardiomyocytes (CMs) is retained in neonatal mouse hearts but is limited in adult mouse hearts. Myocardial infarction (MI) in adult hearts usually leads to the loss of large amounts of cardiac tissue, and then accelerates the process of cardiac remodeling and heart failure. Therefore, it is necessary to explore the potential mechanisms of CM regeneration in the neonates and develop potential therapies aimed at promoting CM regeneration and cardiac repair in adults. Currently, studies indicate that a number of mechanisms are involved in neonatal endogenous myocardial regeneration, including cell cycle regulators, transcription factors, non-coding RNA, signaling pathways, acute inflammation, hypoxia, protein kinases, and others. Understanding the mechanisms of regeneration in neonatal CMs after MI provides theoretical support for the studies related to the promotion of heart repair after MI in adult mammals. However, several difficulties in the study of CM regeneration still need to be overcome. This article reviews the potential mechanisms of endogenous CM regeneration in neonatal mouse hearts and discusses possible therapeutic targets and future research directions.
ISSN:0366-6999
2542-5641
DOI:10.1097/CM9.0000000000000693