About this Research Topic
Cardiovascular diseases (CVD) are the leading causes of death worldwide. More people die annually from CVDs than from any other illness. Although diagnosis and treatment approaches have improved, cardiovascular outcome, survival, and prognosis of heart failure (HF) patients remain minimum. A single episode of myocardial infarction (MI) may result in the permanent loss of billion cardiomyocytes (CMs) or more, and as the mammalian heart has limited regenerative capacity, it leads to HF and possibly, death (1-4). Currently, the only therapy to restore heart function is heart transplantation. Due to the limited number of donor organs, heart transplantation is reserved for patients with end-stage heart failure refractory to conservative medical therapy.
Zebrafish, Newts, and even 1-day mice can not regenerate their injured heart by inducing CM proliferation and lost CMs will be replaced with a new one, which restores the cardiac function. The gene expression studies showed the differential expression of cell cycle regulatory genes, mitotic, and growth pathway genes. To mimic the pro-proliferative mechanisms of these lower phylogenetic organisms in the adult mammalian heart have been attempted using modulation of critical genes, molecular pathways, and miRNAs. Cardiac reprogramming is a novel approach for cardiac regeneration where fibroblast can be transdifferentiated into the CMs using cardiac transcription factors, miRNA, and small molecules. While the efficiency of cardiac reprogramming is low, a breakthrough in the increased trans-differentiation efficiency might help to repair the heart. The direct delivery of stem cells or iPSC or iPSC-derived CMs or cell-derived exosomes to the heart is a promising therapeutic strategy for cardiac repair. Recent studies on autologous iPSC-derived CMs that can be delivered to the heart to replace the lost CMs are assuring. Number studies in mice and large animals showed that the delivered iPSC-CMs could survive and be integrated synchronously in the myocardium with the synchronous electromechanical coupling. By exploring gene function and molecular mechanisms, improved gene or cell delivery approaches will help understand cardiac regeneration better and develop a therapeutic approach for ischemic heart diseases.
This Research Topic focuses on recent advances and challenges in exploring cardiac repair, and regeneration, and functional improvement and covers the following topics, but not limited to:
1) Ischemic heart diseases and heart failure.
2) Natural cardiac regeneration- animal models.
3) Molecular mechanism of cardiac repair and regeneration.
4) Cardiomyocyte proliferation- novel targets and molecular mechanism.
5) Cardiac reprogramming.
6) iPSC-CM therapy and cardiac regeneration.
7) Exosomes and cardiac repair.
8) Novel therapeutic strategies to induce cardiac regeneration and cardiac function.
We embrace any articles such as original basic or translational research, opinions, clinical studies, reviews, and methodology manuscripts.
Zebrafish, Newts, and even 1-day mice can not regenerate their injured heart by inducing CM proliferation and lost CMs will be replaced with a new one, which restores the cardiac function. The gene expression studies showed the differential expression of cell cycle regulatory genes, mitotic, and growth pathway genes. To mimic the pro-proliferative mechanisms of these lower phylogenetic organisms in the adult mammalian heart have been attempted using modulation of critical genes, molecular pathways, and miRNAs. Cardiac reprogramming is a novel approach for cardiac regeneration where fibroblast can be transdifferentiated into the CMs using cardiac transcription factors, miRNA, and small molecules. While the efficiency of cardiac reprogramming is low, a breakthrough in the increased trans-differentiation efficiency might help to repair the heart. The direct delivery of stem cells or iPSC or iPSC-derived CMs or cell-derived exosomes to the heart is a promising therapeutic strategy for cardiac repair. Recent studies on autologous iPSC-derived CMs that can be delivered to the heart to replace the lost CMs are assuring. Number studies in mice and large animals showed that the delivered iPSC-CMs could survive and be integrated synchronously in the myocardium with the synchronous electromechanical coupling. By exploring gene function and molecular mechanisms, improved gene or cell delivery approaches will help understand cardiac regeneration better and develop a therapeutic approach for ischemic heart diseases.
This Research Topic focuses on recent advances and challenges in exploring cardiac repair, and regeneration, and functional improvement and covers the following topics, but not limited to:
1) Ischemic heart diseases and heart failure.
2) Natural cardiac regeneration- animal models.
3) Molecular mechanism of cardiac repair and regeneration.
4) Cardiomyocyte proliferation- novel targets and molecular mechanism.
5) Cardiac reprogramming.
6) iPSC-CM therapy and cardiac regeneration.
7) Exosomes and cardiac repair.
8) Novel therapeutic strategies to induce cardiac regeneration and cardiac function.
We embrace any articles such as original basic or translational research, opinions, clinical studies, reviews, and methodology manuscripts.
Keywords: Cardiomyocyte proliferation, Cardiac reprograming, Stem cells, Cardiovascular diseases, Cardiac regeneration and Exosomes
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