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.

Research Programme

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.  


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Tremendous paper published on a potential mechanism for COVID-19 disease pathogenesis by the group of Prof. Mauro Giacca (King's College)

Paper abstract:

COVID-19 is a disease with unique characteristics that include lung thrombosis, frequent diarrhoea, abnormal activation of the inflammatory response and rapid deterioration of lung function consistent with alveolar oedema. The pathological substrate for these findings remains unknown. Here we show that the lungs of patients with COVID-19 contain infected pneumocytes with abnormal morphology and frequent multinucleation. The generation of these syncytia results from activation of the SARS-CoV-2 spike protein at the cell plasma membrane level. On the basis of these observations, we performed two high-content microscopy-based screenings with more than 3,000 approved drugs to search for inhibitors of spike-driven syncytia. We converged on the identification of 83 drugs that inhibited spike-mediated cell fusion, several of which belonged to defined pharmacological classes. We focused our attention on effective drugs that also protected against virus replication and associated cytopathicity. One of the most effective molecules was the antihelminthic drug niclosamide, which markedly blunted calcium oscillations and membrane conductance in spike-expressing cells by suppressing the activity of TMEM16F (also known as anoctamin 6), a calcium-activated ion channel and scramblase that is responsible for exposure of phosphatidylserine on the cell surface. These findings suggest a potential mechanism for COVID-19 disease pathogenesis and support the repurposing of niclosamide for therapy.

You can access the full paper HERE.