The TRAIN-HEART consortium, funded by the European Commission (2019-2023), is made up to train a league of 15 promising fellows that harness novel insights in the pathogenesis of ischemic heart failure, study the therapeutic potential of existing RNA therapeutics and improve its efficacy by the design of novel drug delivery systems.
TRAIN-HEART brings together leading academic teams and (biotech) companies covering various disciplines ranging from fundamental research to clinical pharmacology and gene therapy to drug delivery applications, have teamed up in the European Union.
The TRAIN-HEART network aims to gain viable insight in the pathogenesis of ischemic heart failure which will serve as a basis for drug discovery and drug delivery efforts that aim to therapeutically target specific molecules and mechanisms within cardiomyocytes for the treatment of ischemic heart failure.
If you have any questions you can fill in the form or mail us directly: info@train-heart.eu.
News
Gene expression is needed for the maintenance of heart function under normal conditions and in response to stress. Each cell type of the heart has a specific program controlling transcription. Different types of stress induce modifications of these programs and, if prolonged, can lead to altered cardiac phenotype and, eventually, to heart failure. The transcriptional status of a gene is regulated by the epigenome, a complex network of DNA and histone modifications. Until a few years ago, our understanding of the role of the epigenome in heart disease was limited to that played by histone deacetylation. But over the last decade, the consequences for the maintenance of homeostasis in the heart and for the development of cardiac hypertrophy of a number of other modifications, including DNA methylation and hydroxymethylation, histone methylation and acetylation, and changes in chromatin architecture, have become better understood. Indeed, it is now clear that many levels of regulation contribute to defining the epigenetic landscape required for correct cardiomyocyte function, and that their perturbation is responsible for cardiac hypertrophy and fibrosis. Here, we review these aspects and draw a picture of what epigenetic modification may imply at the therapeutic level for heart failure.
Access the full article: https://doi.org/10.1152/physrev.00037.2019
Thu, 28 April
This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 813716.
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