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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Cellular reprogramming of fibroblasts in heart regeneration
1Division of Cardiology, Department of Medicine, The University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.
Insights
Cardiac fibroblasts can be reprogrammed into various cardiac cells to regenerate heart tissue after myocardial infarction. This review explores fibroblast reprogramming strategies for heart repair, addressing current limitations and future challenges.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Cellular Reprogramming
Background:
- Myocardial infarction leads to cardiomyocyte loss and fibrosis, causing cardiac dysfunction and heart failure.
- Current therapies only slow disease progression and cannot fully restore heart function due to limited cardiomyocyte regeneration.
- Resident cardiac fibroblasts play crucial roles in heart structure and contractility and are key targets for cardiac repair.
Purpose of the Study:
- To review fibroblast reprogramming strategies for heart regeneration after myocardial infarction.
- To summarize recent findings on using fibroblast-derived cells for cardiac repair.
- To discuss the limitations and challenges in fibroblast-based heart regeneration therapies.
Main Methods:
- Review of scientific literature on fibroblast plasticity and reprogramming.
- Analysis of strategies including fibroblast conversion into induced cardiomyocytes and progenitor cells.
- Examination of stem cell-derived cardiomyocyte transplantation and cardiomyocyte proliferation stimulation.
Main Results:
- Fibroblast plasticity allows reprogramming into induced pluripotent stem cells, cardiac progenitor cells, and cardiomyocytes.
- Fibroblast-derived cells show potential for repairing damaged heart tissue and restoring cardiac function.
- Recent advancements highlight the therapeutic promise of utilizing fibroblast-derived cells for heart regeneration.
Conclusions:
- Fibroblast reprogramming offers a promising avenue for regenerating the damaged heart.
- Further research is needed to overcome limitations and challenges for clinical application.
- Fibroblast-derived cell therapies hold significant potential for treating heart failure post-myocardial infarction.
Abstract:
Myocardial infarction causes the loss of cardiomyocytes and the formation of cardiac fibrosis due to the activation of cardiac fibroblasts, leading to cardiac dysfunction and heart failure. Unfortunately, current therapeutic interventions can only slow the disease progression. Furthermore, they cannot fully restore cardiac function, likely because the adult human heart lacks sufficient capacity to regenerate cardiomyocytes. Therefore, intensive efforts have focused on developing therapeutics to regenerate the damaged heart. Several strategies have been intensively investigated, including stimulation of cardiomyocyte proliferation, transplantation of stem cell-derived cardiomyocytes, and conversion of fibroblasts into cardiac cells. Resident cardiac fibroblasts are critical in the maintenance of the structure and contractility of the heart. Fibroblast plasticity makes this type of cells be reprogrammed into many cell types, including but not limited to induced pluripotent stem cells, induced cardiac progenitor cells, and induced cardiomyocytes. Fibroblasts have become a therapeutic target due to their critical roles in cardiac pathogenesis. This review summarizes the reprogramming of fibroblasts into induced pluripotent stem cell-derived cardiomyocytes, induced cardiac progenitor cells, and induced cardiomyocytes to repair a damaged heart, outlines recent findings in utilizing fibroblast-derived cells for heart regeneration, and discusses the limitations and challenges.
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