Abstract: Markers of an intense scarring process in the early phase post-myocardial infarction (MI) are still undetermined, and the identification of patients at higher risk of developing large adverse fibrotic remodeling and heart failure remains challenging. Here, the inventors demonstrate the modulation in the paracrine behavior of resident PW1+ cells in scarring cardiac tissue post-MI and the differential abundance of 12 candidate markers in their secretome. Of these, growth differentiation factor 3 (GDF3), a member of transforming growth factor-? family, upregulates proliferation of cardiac fibroblasts, which are instrumental in fibrosis. GDF3 is upregulated in the scarred tissue and plasma of mice and humans post-MI, with the highest plasma levels predicting higher fibrotic cardiac remodeling and cardiac dilation.

Abstract: Activated cardiac fibroblasts are essential for the production of extracellular matrix proteins that accumulate during cardiac fibrosis, and PW1+ cardiac adult stem cells were recently proposed as a cellular source of fibroblasts in the ischemic hearts. Here the inventors identify ?V-integrin (or CD51) as an essential regulator of PW1+ cardiac adult stem cells fibrogenic behavior. Inhibition of ?V-integrin reduce the profibrotic gene expression profile and the ability to differentiate into fibroblasts of cardiac PW1+ cells. The pharmacological blockade of ?V-containing integrins improved cardiac function and survival after MI by reducing infarct size and attenuating the extension of reactive cardiac fibrosis. Notably, the total cardiac fibrotic area as well as interstitial fibrosis in the remote myocardial area are significantly reduced after pharmacological blockade of ?V-containing integrins.

Abstract: The present invention relates to the field of cardiology and, more specifically, to a novel algorithm that can be used, in particular, in a method for determining if a drug is likely to induce a cardiac ventricular repolarisation disturbance, based on variations in electrocardiogram data.

Abstract: The present invention relates to the field of cardiology and, more specifically, to a novel algorithm that can be used, in particular, in a method for determining if a drug is likely to induce a cardiac ventricular repolarisation disturbance, based on variations in electrocardiogram data.

Abstract: The invention relates to inhibitors of Multi drug Resistant Protein 4 (MRP4) for the treatment and/or the prevention of cardiac disorders, such as acute or chronic heart failure and cardiogenic shock. The invention also relates to agents stimulating MRP4 activity for the treatment and/or the prevention of cardiac hypertrophy.

Abstract: The invention relates to inhibitors of MRP4 for the treatment and/or the prevention of vascular disorders such as atherosclerosis, post-angioplasty restenosis, pulmonary arterial hypertension or vein-graft disease.

Abstract: The invention relates to inhibitors of Multi drug Resistant Protein 4 (MRP4) for the treatment and/or the prevention of cardiac disorders, such as acute or chronic heart failure and cardiogenic shock. The invention also relates to agents stimulating MRP4 activity for the treatment and/or the prevention of cardiac hypertrophy.

Abstract: The invention relates to inhibitors of STIM1 for the treatment and/or the prevention of cardiac disorders such as atherosclerosis, post-angioplasty restenosis, pulmonary arterial hypertension, vein-graft disease, cardiac hypertrophy, cardiac arrhythmias, valvulopathies, diastolic dysfunction, chronic heart failure, ischemic heart failure, and myocarditis.

Abstract: The invention relates to inhibitors of MRP4 for the treatment and/or the prevention of vascular disorders such as atherosclerosis, post-angioplasty restenosis, pulmonary arterial hypertension or vein-graft disease.