Exploring the Regulation Mechanism of Cardiomyocyte Proliferation and Cardiac Regeneration
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Proliferation and Division".
Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 4013
Special Issue Editors
Interests: molecular regulatory mechanism; stem cell; cardiovascular disease; translational and regenerative medicine
Interests: cardiomyocyte; cell cycle; regeneration; cardiotoxicity; nanoparticle
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
As we know, Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide. Apoptosis, necrosis, and autophagy occur in cardiac myocytes, and both gradual and acute cell death are hallmarks of cardiac pathology, including heart failure, myocardial infarction (MI), and ischemia/reperfusion. According to traditional concepts, adult cardiomyocytes (CMs) are non-renewable cells. Repairing and replenishing damaged and missing CMs has become a fundamental strategy to improve survival in patients with CVD. Previous studies have shown that some neonatal mammalian hearts can self-repair after injury through the proliferation of their own CMs, thereby achieving cardiac regeneration. However, during postnatal cardiac development, the ability of CMs to proliferate is gradually lost, rendering the adult mammalian heart unable to repair itself after injury. In recent years, some studies have reported that some chemicals and targeted gene therapy can promote the proliferation of adult CMs to a certain extent. Thus, promoting endogenous cardiomyocyte (CM) proliferation may compensate for lost myocardial cells, repair damaged heart tissue, and improve cardiac functions, which has become a new strategy for cardiac regeneration after CVDs. Two cardioprotective chemicals, FGF1 and CHIR99021, were previously identified. They are proven to promote the proliferation of cardiomyocytes derived from human pluripotent stem cells (iPSC-CMs) and confer cardioprotection in the mouse and pig models of acute myocardial infarction. Mechanisms underlying cardiomyocyte proliferation and cardiac regeneration remain elusive.
In this Special Issue, we aim to investigate the underlying mechanism of cardiomyocyte proliferation and cardiac regeneration, including both clinical and basic studies. For the basic studies, we accept different types of related research, you can study the mechanism using different disease models including various cell, tissue, and animal models. We would like to present scientific advances in the therapeutic strategies of CVDs in cardiac regeneration, including novel data in relevant animals and humans. We welcome all scientists working in the heart regeneration field to participate in this Special Issue and submit high-quality original research. This will bring excellent prospects for patients who suffer from myocardial injury.
Dr. Ling Tang
Dr. Wuqiang Zhu
Guest Editors
Manuscript Submission Information
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Keywords
- cardiovascular disease
- cardiomyocyte proliferation and cardiac regeneration
- underlying mechanism
- disease model
- compensate for lost myocardial cells
- repair damaged heart tissue
- improve cardiac functions
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