Modulation of connective tissue growth factor and activin receptor 2B function in cardiac hypertrophy and fibrosis

The increase of cardiac hemodynamic load that requires increased mechanical performance drives adaptation of the heart to maintain cardiac function. Modification of protein synthesis in cardiomyocytes allows the cells to adapt to the increased load. Cardiomyocyte hypertrophy and activation of cardiac fibroblasts over the long term is maladaptive and leads to heart failure (HF). Understanding the complex and converging pathways regulating cardiac remodeling is a major challenge, but it may allow for opportunities to develop new therapies, new medicines and provide new hope for people with these life-threatening diseases.