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Journal articles on the topic 'Direct cardiac reprogramming'

Author: Grafiati

Published: 8 June 2024

Last updated: 19 July 2025

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1

Qian, Li, and Deepak Srivastava. "Direct Cardiac Reprogramming." Circulation Research 113, no. 7 (2013): 915–21. http://dx.doi.org/10.1161/circresaha.112.300625.

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2

Sadahiro, Taketaro, Shinya Yamanaka, and Masaki Ieda. "Direct Cardiac Reprogramming." Circulation Research 116, no. 8 (2015): 1378–91. http://dx.doi.org/10.1161/circresaha.116.305374.

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3

Bruneau, Benoit G. "Direct Reprogramming for Cardiac Regeneration." Circulation Research 110, no. 11 (2012): 1392–94. http://dx.doi.org/10.1161/circresaha.112.270637.

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4

Kim, Junyeop, Yujung Chang, Yerim Hwang, Sumin Kim, Yu-Kyoung Oh, and Jongpil Kim. "Graphene Nanosheets Mediate Efficient Direct Reprogramming into Induced Cardiomyocytes." Journal of Biomedical Nanotechnology 18, no. 9 (2022): 2171–82. http://dx.doi.org/10.1166/jbn.2022.3416.

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In vivo cardiac reprogramming is a potential therapeutic strategy to replace cardiomyocytes in patients with myocardial infarction. However, low conversion efficiency is a limitation of In vivo cardiac reprogramming for heart failure. In this study, we showed that graphene nanosheets mediated efficient direct reprogramming into induced cardiomyocytes In vivo. We observed that the administration of graphene nanosheets led to the accumulation of H3K4me3, which resulted in direct cardiac reprogramming. Importantly, the administration of graphene nanosheets combined with cardiac reprogramming fact

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5

Chen, Olivia, and Li Qian. "Direct Cardiac Reprogramming: Advances in Cardiac Regeneration." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/580406.

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Heart disease is one of the lead causes of death worldwide. Many forms of heart disease, including myocardial infarction and pressure-loading cardiomyopathies, result in irreversible cardiomyocyte death. Activated fibroblasts respond to cardiac injury by forming scar tissue, but ultimately this response fails to restore cardiac function. Unfortunately, the human heart has little regenerative ability and long-term outcomes following acute coronary events often include chronic and end-stage heart failure. Building upon years of research aimed at restoring functional cardiomyocytes, recent advanc

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Zhang, Zhentao, Jesse Villalpando, Wenhui Zhang, and Young-Jae Nam. "Chamber-Specific Protein Expression during Direct Cardiac Reprogramming." Cells 10, no. 6 (2021): 1513. http://dx.doi.org/10.3390/cells10061513.

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Forced expression of core cardiogenic transcription factors can directly reprogram fibroblasts to induced cardiomyocyte-like cells (iCMs) in vitro and in vivo. This cardiac reprogramming approach provides a proof of concept for induced heart regeneration by converting a fibroblast fate to a cardiomyocyte fate. However, it remains elusive whether chamber-specific cardiomyocytes can be generated by cardiac reprogramming. Therefore, we assessed the ability of the cardiac reprogramming approach for chamber specification in vitro and in vivo. We found that in vivo cardiac reprogramming post-myocard

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Ambroise, Rachelle, Paige Takasugi, Jiandong Liu, and Li Qian. "Direct Cardiac Reprogramming in the Age of Computational Biology." Journal of Cardiovascular Development and Disease 11, no. 9 (2024): 273. http://dx.doi.org/10.3390/jcdd11090273.

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Heart disease continues to be one of the most fatal conditions worldwide. This is in part due to the maladaptive remodeling process by which ischemic cardiac tissue is replaced with a fibrotic scar. Direct cardiac reprogramming presents a unique solution for restoring injured cardiac tissue through the direct conversion of fibroblasts into induced cardiomyocytes, bypassing the transition through a pluripotent state. Since its inception in 2010, direct cardiac reprogramming using the transcription factors Gata4, Mef2c, and Tbx5 has revolutionized the field of cardiac regenerative medicine. Just

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8

Tani, Hidenori, Taketaro Sadahiro, and Masaki Ieda. "Direct Cardiac Reprogramming: A Novel Approach for Heart Regeneration." International Journal of Molecular Sciences 19, no. 9 (2018): 2629. http://dx.doi.org/10.3390/ijms19092629.

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Cardiac diseases are among the most common causes of death globally. Cardiac muscle has limited proliferative capacity, and regenerative therapies are highly in demand as a new treatment strategy. Although pluripotent reprogramming has been developed, it has obstacles, such as a potential risk of tumor formation, poor survival of the transplanted cells, and high cost. We previously reported that fibroblasts can be directly reprogrammed to cardiomyocytes by overexpressing a combination of three cardiac-specific transcription factors (Gata4, Mef2c, Tbx5 (together, GMT)). We and other groups have

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9

Tang, Yawen, Sajesan Aryal, Xiaoxiao Geng, et al. "TBX20 Improves Contractility and Mitochondrial Function During Direct Human Cardiac Reprogramming." Circulation 146, no. 20 (2022): 1518–36. http://dx.doi.org/10.1161/circulationaha.122.059713.

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Background: Direct cardiac reprogramming of fibroblasts into cardiomyocytes has emerged as a promising strategy to remuscularize injured myocardium. However, it is insufficient to generate functional induced cardiomyocytes from human fibroblasts using conventional reprogramming cocktails, and the underlying molecular mechanisms are not well studied. Methods: To discover potential missing factors for human direct reprogramming, we performed transcriptomic comparison between human induced cardiomyocytes and functional cardiomyocytes. Results: We identified TBX20 (T-box transcription factor 20) a

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10

Perveen, Sadia, Roberto Vanni, Marco Lo Iacono, Raffaella Rastaldo, and Claudia Giachino. "Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration." Cells 12, no. 8 (2023): 1166. http://dx.doi.org/10.3390/cells12081166.

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Cardiac diseases are the foremost cause of morbidity and mortality worldwide. The heart has limited regenerative potential; therefore, lost cardiac tissue cannot be replenished after cardiac injury. Conventional therapies are unable to restore functional cardiac tissue. In recent decades, much attention has been paid to regenerative medicine to overcome this issue. Direct reprogramming is a promising therapeutic approach in regenerative cardiac medicine that has the potential to provide in situ cardiac regeneration. It consists of direct cell fate conversion of one cell type into another, avoi

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11

Sadahiro, Taketaro. "Direct Cardiac Reprogramming ― Converting Cardiac Fibroblasts to Cardiomyocytes ―." Circulation Reports 1, no. 12 (2019): 564–67. http://dx.doi.org/10.1253/circrep.cr-19-0104.

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12

Ieda, Masaki. "Direct cardiac reprogramming by defined factors." Inflammation and Regeneration 33, no. 4 (2013): 190–96. http://dx.doi.org/10.2492/inflammregen.33.190.

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13

Engel, James L., and Reza Ardehali. "Direct Cardiac Reprogramming: Progress and Promise." Stem Cells International 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/1435746.

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The human adult heart lacks a robust endogenous repair mechanism to fully restore cardiac function after insult; thus, the ability to regenerate and repair the injured myocardium remains a top priority in treating heart failure. The ability to efficiently generate a large number of functioning cardiomyocytes capable of functional integration within the injured heart has been difficult. However, the ability to directly convert fibroblasts into cardiomyocyte-like cells both in vitro and in vivo offers great promise in overcoming this problem. In this review, we describe the insights and progress

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14

Kurotsu, Shota, Takeshi Suzuki, and Masaki Ieda. "Mechanical stress regulates cardiac direct reprogramming." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): OR15–1. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_or15-1.

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15

Osakabe, Rina, Takeshi Suzuki, and Masaki Ieda. "Heart repair using direct cardiac reprogramming." Folia Pharmacologica Japonica 150, no. 6 (2017): 276–81. http://dx.doi.org/10.1254/fpj.150.276.

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16

Srivastava, Deepak, and Penghzi Yu. "Recent advances in direct cardiac reprogramming." Current Opinion in Genetics & Development 34 (October 2015): 77–81. http://dx.doi.org/10.1016/j.gde.2015.09.004.

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17

Ieda, Masaki. "Direct Cardiac Reprogramming for Regenerative Medicine." Journal of Cardiac Failure 21, no. 10 (2015): S160. http://dx.doi.org/10.1016/j.cardfail.2015.08.093.

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18

Kurotsu, Shota, Takeshi Suzuki, and Masaki Ieda. "Direct Reprogramming, Epigenetics, and Cardiac Regeneration." Journal of Cardiac Failure 23, no. 7 (2017): 552–57. http://dx.doi.org/10.1016/j.cardfail.2017.05.009.

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19

Vaseghi, Haley, Jiandong Liu, and Li Qian. "Molecular barriers to direct cardiac reprogramming." Protein & Cell 8, no. 10 (2017): 724–34. http://dx.doi.org/10.1007/s13238-017-0402-x.

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20

Bektik, Emre, and Ji-dong Fu. "Ameliorating the Fibrotic Remodeling of the Heart through Direct Cardiac Reprogramming." Cells 8, no. 7 (2019): 679. http://dx.doi.org/10.3390/cells8070679.

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Coronary artery disease is the most common form of cardiovascular diseases, resulting in the loss of cardiomyocytes (CM) at the site of ischemic injury. To compensate for the loss of CMs, cardiac fibroblasts quickly respond to injury and initiate cardiac remodeling in an injured heart. In the remodeling process, cardiac fibroblasts proliferate and differentiate into myofibroblasts, which secrete extracellular matrix to support the intact structure of the heart, and eventually differentiate into matrifibrocytes to form chronic scar tissue. Discovery of direct cardiac reprogramming offers a prom

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21

Wang, Li, Hong Ma, Peisen Huang, et al. "Down-regulation of Beclin1 promotes direct cardiac reprogramming." Science Translational Medicine 12, no. 566 (2020): eaay7856. http://dx.doi.org/10.1126/scitranslmed.aay7856.

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Direct reprogramming of fibroblasts to alternative cell fates by forced expression of transcription factors offers a platform to explore fundamental molecular events governing cell fate identity. The discovery and study of induced cardiomyocytes (iCMs) not only provides alternative therapeutic strategies for heart disease but also sheds lights on basic biology underlying CM fate determination. The iCM field has primarily focused on early transcriptome and epigenome repatterning, whereas little is known about how reprogramming iCMs remodel, erase, and exit the initial fibroblast lineage to acqu

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22

Muniyandi, Priyadharshni, Toru Maekawa, Tatsuro Hanajiri, and Vivekanandan Palaninathan. "Direct Cardiac Reprogramming with Engineered miRNA Scaffolds." Current Pharmaceutical Design 26, no. 34 (2020): 4285–303. http://dx.doi.org/10.2174/1381612826666200327161112.

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Ischemic heart disease is a predominant cause of death worldwide. The loss or death of cardiomyocytes due to restricted blood flow often results in a cardiac injury. Myofibroblasts replace these injured cardiomyocytes to preserve structural integrity. However, the depleted cardiomyocytes lead to cardiac dysfunction such as pathological cardiac dilation, reduced cardiac contraction, and fibrosis. Repair and regeneration of myocardium are the best possible therapy for end-stage heart failure patients because the current cardiomyocytes restoration therapies are limited to heart transplantation on

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23

Song, Seuk Young, Jin Yoo, Seokhyeong Go, et al. "Cardiac-mimetic cell-culture system for direct cardiac reprogramming." Theranostics 9, no. 23 (2019): 6734–44. http://dx.doi.org/10.7150/thno.35574.

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24

Paoletti, Camilla, Elena Marcello, Maria Luna Melis, Carla Divieto, Daria Nurzynska, and Valeria Chiono. "Cardiac Tissue-like 3D Microenvironment Enhances Route towards Human Fibroblast Direct Reprogramming into Induced Cardiomyocytes by microRNAs." Cells 11, no. 5 (2022): 800. http://dx.doi.org/10.3390/cells11050800.

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The restoration of cardiac functionality after myocardial infarction represents a major clinical challenge. Recently, we found that transient transfection with microRNA combination (miRcombo: miR-1, miR-133, miR-208 and 499) is able to trigger direct reprogramming of adult human cardiac fibroblasts (AHCFs) into induced cardiomyocytes (iCMs) in vitro. However, achieving efficient direct reprogramming still remains a challenge. The aim of this study was to investigate the influence of cardiac tissue-like biochemical and biophysical stimuli on direct reprogramming efficiency. Biomatrix (BM), a ca

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25

Doppler, Stefanie, Marcus-André Deutsch, Rüdiger Lange, and Markus Krane. "Direct Reprogramming—The Future of Cardiac Regeneration?" International Journal of Molecular Sciences 16, no. 8 (2015): 17368–93. http://dx.doi.org/10.3390/ijms160817368.

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26

Kojima, Hidenori, and Masaki Ieda. "Discovery and progress of direct cardiac reprogramming." Cellular and Molecular Life Sciences 74, no. 12 (2017): 2203–15. http://dx.doi.org/10.1007/s00018-017-2466-4.

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27

Talkhabi, Mahmood, Elmira Rezaei Zonooz, and Hossein Baharvand. "Boosters and barriers for direct cardiac reprogramming." Life Sciences 178 (June 2017): 70–86. http://dx.doi.org/10.1016/j.lfs.2017.04.013.

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28

Wang, Li, Peisen Huang, David Near, et al. "Isoform Specific Effects of Mef2C during Direct Cardiac Reprogramming." Cells 9, no. 2 (2020): 268. http://dx.doi.org/10.3390/cells9020268.

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Direct conversion of cardiac fibroblasts into induced cardiomyocytes (iCMs) by forced expression of defined factors holds great potential for regenerative medicine by offering an alternative strategy for treatment of heart disease. Successful iCM conversion can be achieved by minimally using three transcription factors, Mef2c (M), Gata4(G), and Tbx5 (T). Despite increasing interest in iCM mechanistic studies using MGT(polycistronic construct with optimal expression of M,G and T), the reprogramming efficiency varies among different laboratories. Two main Mef2c isoforms (isoform2, Mi2 and isofor

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29

Xiong, Ziyan, and Yuanlin Lei. "Research Progress and Prospects of Direct Cardiac Reprogramming Technology." Journal of Contemporary Medical Practice 7, no. 4 (2025): 26–29. https://doi.org/10.53469/jcmp.2025.07(04).06.

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As adult cardiomyocytes are in a state of terminal differentiation, they have no regenerative capacity. Once the heart is subjected to ischemia and hypoxia, cardiomyocytes suffer irreversible damage, and damaged and necrotic cardiomyocytes are replaced by myocardial fibroblasts, which in turn form scar tissue leading to cardiac remodeling and ultimately to heart failure. The discovery of direct cardiac reprogramming, in which myocardial fibroblasts are induced to become cardiomyocyte-like cells by specific means, holds new promise for the treatment of cardiac diseases and the regeneration of t

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30

Passaro, Fabiana, Gianluca Testa, Luigi Ambrosone, et al. "Nanotechnology-Based Cardiac Targeting and Direct Cardiac Reprogramming: The Betrothed." Stem Cells International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/4940397.

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Cardiovascular diseases represent the first cause of morbidity in Western countries, and chronic heart failure features a significant health care burden in developed countries. Efforts in the attempt of finding new possible strategies for the treatment of CHF yielded several approaches based on the use of stem cells. The discovery of direct cardiac reprogramming has unveiled a new approach to heart regeneration, allowing, at least in principle, the conversion of one differentiated cell type into another without proceeding through a pluripotent intermediate. First developed for cancer treatment

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31

Adams, Emma, Rachel McCloy, Ashley Jordan, Kaitlin Falconer, and Iain M. Dykes. "Direct Reprogramming of Cardiac Fibroblasts to Repair the Injured Heart." Journal of Cardiovascular Development and Disease 8, no. 7 (2021): 72. http://dx.doi.org/10.3390/jcdd8070072.

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Coronary heart disease is a leading cause of mortality and morbidity. Those that survive acute myocardial infarction are at significant risk of subsequent heart failure due to fibrotic remodelling of the infarcted myocardium. By applying knowledge from the study of embryonic cardiovascular development, modern medicine offers hope for treatment of this condition through regeneration of the myocardium by direct reprogramming of fibrotic scar tissue. Here, we will review mechanisms of cell fate specification leading to the generation of cardiovascular cell types in the embryo and use this as a fr

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32

Ghazizadeh, Z., H. Rassouli, H. Fonoudi, et al. "Direct reprogramming of human fibroblasts to a cardiac fate using reprogramming proteins." Cytotherapy 16, no. 4 (2014): S39. http://dx.doi.org/10.1016/j.jcyt.2014.01.134.

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33

Baksh, Syeda Samara, and Conrad P. Hodgkinson. "Conservation of miR combo based direct cardiac reprogramming." Biochemistry and Biophysics Reports 31 (September 2022): 101310. http://dx.doi.org/10.1016/j.bbrep.2022.101310.

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34

Guo, Chuner, Kishan Patel, and Li Qian. "Direct Somatic Cell Reprogramming: Treatment of Cardiac Diseases." Current Gene Therapy 13, no. 2 (2013): 133–38. http://dx.doi.org/10.2174/1566523211313020007.

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35

Guo, Chuner, Kishan Patel, and Li Qian. "Direct Somatic Cell Reprogramming: Treatment of Cardiac Diseases." Current Gene Therapy 999, no. 999 (2013): 1–7. http://dx.doi.org/10.2174/15665232113139990023.

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36

Sadahiro, Taketaro, and Masaki Ieda. "Direct Cardiac Reprogramming for Cardiovascular Regeneration and Differentiation." Keio Journal of Medicine 69, no. 3 (2020): 49–58. http://dx.doi.org/10.2302/kjm.2019-0008-oa.

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37

Garbutt, Tiffany A., Yang Zhou, Benjamin Keepers, Jiandong Liu, and Li Qian. "An Optimized Protocol for Human Direct Cardiac Reprogramming." STAR Protocols 1, no. 1 (2020): 100010. http://dx.doi.org/10.1016/j.xpro.2019.100010.

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38

Inagawa, Kohei, and Masaki Ieda. "Direct Reprogramming of Mouse Fibroblasts into Cardiac Myocytes." Journal of Cardiovascular Translational Research 6, no. 1 (2012): 37–45. http://dx.doi.org/10.1007/s12265-012-9412-5.

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39

Batty, Jonathan A., Jose A. C. Lima, and Vijay Kunadian. "Direct cellular reprogramming for cardiac repair and regeneration." European Journal of Heart Failure 18, no. 2 (2015): 145–56. http://dx.doi.org/10.1002/ejhf.446.

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40

Yamada, Yu, Taketaro Sadahiro, and Masaki Ieda. "Development of direct cardiac reprogramming for clinical applications." Journal of Molecular and Cellular Cardiology 178 (May 2023): 1–8. http://dx.doi.org/10.1016/j.yjmcc.2023.03.002.

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41

Bektik, Emre, Yu Sun, Adrienne T. Dennis, et al. "Inhibition of CREB-CBP Signaling Improves Fibroblast Plasticity for Direct Cardiac Reprogramming." Cells 10, no. 7 (2021): 1572. http://dx.doi.org/10.3390/cells10071572.

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Direct cardiac reprogramming of fibroblasts into induced cardiomyocytes (iCMs) is a promising approach but remains a challenge in heart regeneration. Efforts have focused on improving the efficiency by understanding fundamental mechanisms. One major challenge is that the plasticity of cultured fibroblast varies batch to batch with unknown mechanisms. Here, we noticed a portion of in vitro cultured fibroblasts have been activated to differentiate into myofibroblasts, marked by the expression of αSMA, even in primary cell cultures. Both forskolin, which increases cAMP levels, and TGFβ inhibitor

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42

Liu, Liu, Yijing Guo, Zhaokai Li, and Zhong Wang. "Improving Cardiac Reprogramming for Heart Regeneration in Translational Medicine." Cells 10, no. 12 (2021): 3297. http://dx.doi.org/10.3390/cells10123297.

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Direct reprogramming of fibroblasts into CM-like cells has emerged as an attractive strategy to generate induced CMs (iCMs) in heart regeneration. However, low conversion rate, poor purity, and the lack of precise conversion of iCMs are still present as significant challenges. In this review, we summarize the recent development in understanding the molecular mechanisms of cardiac reprogramming with various strategies to achieve more efficient iCMs. reprogramming. Specifically, we focus on the identified critical roles of transcriptional regulation, epigenetic modification, signaling pathways f

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43

López-Muneta, Leyre, Josu Miranda-Arrubla, and Xonia Carvajal-Vergara. "The Future of Direct Cardiac Reprogramming: Any GMT Cocktail Variety?" International Journal of Molecular Sciences 21, no. 21 (2020): 7950. http://dx.doi.org/10.3390/ijms21217950.

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Direct cardiac reprogramming has emerged as a novel therapeutic approach to treat and regenerate injured hearts through the direct conversion of fibroblasts into cardiac cells. Most studies have focused on the reprogramming of fibroblasts into induced cardiomyocytes (iCMs). The first study in which this technology was described, showed that at least a combination of three transcription factors, GATA4, MEF2C and TBX5 (GMT cocktail), was required for the reprogramming into iCMs in vitro using mouse cells. However, this was later demonstrated to be insufficient for the reprogramming of human cell

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44

Zhou, Yang, Sahar Alimohamadi, Li Wang, et al. "A Loss of Function Screen of Epigenetic Modifiers and Splicing Factors during Early Stage of Cardiac Reprogramming." Stem Cells International 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/3814747.

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Direct reprogramming of cardiac fibroblasts (CFs) to induced cardiomyocytes (iCMs) is a newly emerged promising approach for cardiac regeneration, disease modeling, and drug discovery. However, its potential has been drastically limited due to the low reprogramming efficiency and largely unknown underlying molecular mechanisms. We have previously screened and identified epigenetic factors related to histone modification during iCM reprogramming. Here, we used shRNAs targeting an additional battery of epigenetic factors involved in chromatin remodeling and RNA splicing factors to further identi

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45

Muniyandi, Priyadharshni, Vivekanandan Palaninathan, Tatsuro Hanajiri, and Toru Maekawa. "Direct Cardiac Epigenetic Reprogramming through Codelivery of 5′Azacytidine and miR-133a Nanoformulation." International Journal of Molecular Sciences 23, no. 23 (2022): 15179. http://dx.doi.org/10.3390/ijms232315179.

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Direct reprogramming of cardiac fibroblasts to induced cardiomyocytes (iCMs) is a promising approach to cardiac regeneration. However, the low yield of reprogrammed cells and the underlying epigenetic barriers limit its potential. Epigenetic control of gene regulation is a primary factor in maintaining cellular identities. For instance, DNA methylation controls cell differentiation in adults, establishing that epigenetic factors are crucial for sustaining altered gene expression patterns with subsequent rounds of cell division. This study attempts to demonstrate that 5′AZA and miR-133a encapsu

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46

Engel, James L., and Reza Ardehali. "Sendai virus based direct cardiac reprogramming: what lies ahead?" Stem Cell Investigation 5 (October 2018): 37. http://dx.doi.org/10.21037/sci.2018.10.02.

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47

Xie, Yifang, Ben Van Handel, Li Qian, and Reza Ardehali. "Recent advances and future prospects in direct cardiac reprogramming." Nature Cardiovascular Research 2, no. 12 (2023): 1148–58. http://dx.doi.org/10.1038/s44161-023-00377-w.

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48

Tendean, Marshel, Yudi Her Oktaviono, and Ferry Sandra. "Cardiomyocyte Reprogramming: A Potential Strategy for Cardiac Regeneration." Molecular and Cellular Biomedical Sciences 1, no. 1 (2017): 1. http://dx.doi.org/10.21705/mcbs.v1i1.5.

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Heart disease is the leading cause of death worldwide. Within decades a limited process of cardiac cell regeneration was under observation. Embryonic stem cell (ESC) shows great potential for cell and tissue regeneration. Studies indicate that ESC has the potential to enhance myocardial perfusion and/or contractile performance in ischemic myocardium. However there is still challenge to evaluate the issues of teratoma. Then induced pluripotent stem cell was invented by introducing four transcriptional factors (Oct4, Sox2, Klf4, c-Myc). iPSC was created from murine fibroblast and then differenti

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49

Sadahiro, Taketaro. "Cardiac regeneration with pluripotent stem cell-derived cardiomyocytes and direct cardiac reprogramming." Regenerative Therapy 11 (December 2019): 95–100. http://dx.doi.org/10.1016/j.reth.2019.06.004.

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50

Testa, Gianluca, Giorgia Di Benedetto, and Fabiana Passaro. "Advanced Technologies to Target Cardiac Cell Fate Plasticity for Heart Regeneration." International Journal of Molecular Sciences 22, no. 17 (2021): 9517. http://dx.doi.org/10.3390/ijms22179517.

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The adult human heart can only adapt to heart diseases by starting a myocardial remodeling process to compensate for the loss of functional cardiomyocytes, which ultimately develop into heart failure. In recent decades, the evolution of new strategies to regenerate the injured myocardium based on cellular reprogramming represents a revolutionary new paradigm for cardiac repair by targeting some key signaling molecules governing cardiac cell fate plasticity. While the indirect reprogramming routes require an in vitro engineered 3D tissue to be transplanted in vivo, the direct cardiac reprogramm

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