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.