Summary
Cardiovascular diseases are the leading cause of death worldwide, accounting roughly for 45% of all deaths in Europe and costing billions of euros to the European Union economy. Among these, most cardiovascular diseases, such as myocardial infarction, lead to the formation of heart scarring, which is the formation of fibrotic tissue that impairs contractility and cardiac function, ultimately causing heart failure. Despite the prevalence and serious consequences of heart fibrosis, current benchmark therapies have low long-term efficacy, and alternative novel therapies that have reached clinical testing still present severe limitations or lead to little improvement in cardiac function. Thus, there is still an urgent unmet need for the development of novel and efficient therapies for cardiac fibrosis. Cutting-edge research regarding the use of stem cells or delivery of molecules to induce cardiomyocyte proliferation are yet to be successful, as most of these therapies present challenges regarding immunogenicity, efficiency, and long-lasting effect. Thereby, MyoNanoCell project aims at developing a radically new platform for heart fibrosis and cardiac regeneration. By using a combinatory approach, where the MyoNanoCell nanohybrids incorporate not only the ability to carry different cardiomyogenic molecules, but also the ability to modulate the cardiac microenvironment and recognize cardiac fibroblasts, MyoNanoCell will radically increase therapeutic efficiency. Moreover, the simultaneous modulation of cardiac microenvironment and its repopulation with cardiomyocytes by fibroblast reprogramming will directly impact contractility and heart function, representing a paradigm shift in cardiac fibrosis therapy. MyoNanoCell will be fully characterized in vitro to have a full biological fingerprint on the process of cell identity shift, and also tested in advanced 3D in vitro models, to evaluate its overall effects at tissue level.
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| Web resources: | https://cordis.europa.eu/project/id/101146545 |
| Start date: | 01-09-2025 |
| End date: | 31-08-2027 |
| Total budget - Public funding: | - 187 624,00 Euro |
Cordis data
Original description
Cardiovascular diseases are the leading cause of death worldwide, accounting roughly for 45% of all deaths in Europe and costing billions of euros to the European Union economy. Among these, most cardiovascular diseases, such as myocardial infarction, lead to the formation of heart scarring, which is the formation of fibrotic tissue that impairs contractility and cardiac function, ultimately causing heart failure. Despite the prevalence and serious consequences of heart fibrosis, current benchmark therapies have low long-term efficacy, and alternative novel therapies that have reached clinical testing still present severe limitations or lead to little improvement in cardiac function. Thus, there is still an urgent unmet need for the development of novel and efficient therapies for cardiac fibrosis. Cutting-edge research regarding the use of stem cells or delivery of molecules to induce cardiomyocyte proliferation are yet to be successful, as most of these therapies present challenges regarding immunogenicity, efficiency, and long-lasting effect. Thereby, MyoNanoCell project aims at developing a radically new platform for heart fibrosis and cardiac regeneration. By using a combinatory approach, where the MyoNanoCell nanohybrids incorporate not only the ability to carry different cardiomyogenic molecules, but also the ability to modulate the cardiac microenvironment and recognize cardiac fibroblasts, MyoNanoCell will radically increase therapeutic efficiency. Moreover, the simultaneous modulation of cardiac microenvironment and its repopulation with cardiomyocytes by fibroblast reprogramming will directly impact contractility and heart function, representing a paradigm shift in cardiac fibrosis therapy. MyoNanoCell will be fully characterized in vitro to have a full biological fingerprint on the process of cell identity shift, and also tested in advanced 3D in vitro models, to evaluate its overall effects at tissue level.Status
SIGNEDCall topic
HORIZON-MSCA-2023-PF-01-01Update Date
24-11-2024
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