Molecular Biomedicine | Targeting cardiomyocyte proliferation as a key approach of promoting heart repair after injury


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Cardiovascular diseases such as myocardial infarction (MI) is a major contributor to human mortality and morbidity. The mammalian adult heart almost loses its plasticity to appreciably regenerate new cardiomyocytes after injuries, such as MI and heart failure. The neonatal heart exhibits robust proliferative capacity when exposed to varying forms of myocardial damage. The ability of the neonatal heart to repair the injury and prevent pathological left ventricular remodeling leads to preserved or improved cardiac function. Therefore, promoting cardiomyocyte proliferation after injuries to reinitiate the process of cardiomyocyte regeneration, and suppress heart failure and other serious cardiovascular problems have become the primary goal of many researchers. Here, we review recent studies in this field and summarize the factors that act upon the proliferation of cardiomyocytes and cardiac repair after injury and discuss the new possibilities for potential clinical treatment strategies for cardiovascular diseases.

Here, authors present an overview divided into several sections: transcription factors, extracellular matrix, signaling pathways, soluble factors, and microRNAs. In this article, we sort out the latest research advances in each field in cardiac regenerative repair and discuss the controversial contents, which have potential implications for the study of regenerative drugs.

Overview of heart regeneration in mice inside and outside the regeneration window

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