Inhibition of RhoGEF12 leads to considerable improvement in disease progression
The heart responds to the increased stress caused by chronically raised blood pressure, for example, by thickening its wall muscle. In the late stage of this condition, a risk of heart failure arises. Scientists from the Max Planck Institute for Heart and Lung Research have now succeeded in identifying a key molecule in the molecular signalling cascade responsible for this growth. Based on this discovery, they managed to achieve a significant reduction in cardiac wall thickening in animal experiments. In addition, they managed to partly reduce existing thickening of the cardiac wall.
The heart reacts to intensive, long-term stress by increasing its muscle mass. In competitive athletes, this thickening of the cardiac wall is known as athletic heart syndrome or “athlete’s heart”. Whereas in this case, the process is a reversible physiological reaction to physical activity, in other cases, cardiac wall thickening, known medically as cardiac hypertrophy, is a serious condition; its progression frequently leads to death through heart failure. The triggers for this pathological change can include, for example, high blood pressure, arteriosclerosis and cardiac valve defects.