Brain Natriuretic Peptide Protects Cardiomyocytes from Apoptosis and Stimulates Their Cell Cycle Re-Entry in Mouse Infarcted Hearts.

Brain Natriuretic Peptide (BNP) supplementation after infarction increases heart function and decreases heart remodeling. BNP receptors, NPR-A and NPR-B are expressed on adult cardiomyocytes (CMs). We investigated whether a part of the BNP cardioprotective effect in infarcted and unmanipulated hearts is due to modulation of the CM fate.

Increasing heart vascularisation after myocardial infarction using brain natriuretic peptide stimulation of endothelial and WT1 epicardial cells.

Brain natriuretic peptide (BNP) treatment increases heart function and decreases heart dilation after myocardial infarction (MI). Here, we investigated whether part of the cardioprotective effect of BNP in infarcted hearts related to improved neovascularisation. Infarcted mice were treated with saline or BNP for 10 days.

Oxygen as a key regulator of cardiomyocyte proliferation: New results about cell culture conditions!

The goal of the new therapeutically strategies aimed to treat cardiovascular diseases (CVDs) is to enhance the natural ability of the heart to regenerate. This represents a great challenge for the coming years as all the mechanisms underlying the replacement of dying cells by functional cells of the same type are not completely elucidated. Among these, stimulating cardiomyocyte proliferation seems to be crucial for the restoration of normal cardiac function after CVDs.