Scientists at the Max Planck Institute for Heart and Lung Research in Bad Nauheim and Giessen University have discovered that transcription factor Fox01 plays a key role in the development of hypertension.

The researchers were able to cure pulmonary hypertension in rats by activating Fox01, and the findings could be used to develop a new treatment for the condition. A news release from Max-Planck-Gesellschaft indicates that the research team identified a key molecule that plays a role in the regulation of cell division in vascular wall cells and the lifespan of cells.

The research team found an important clue about the central role of Fox01 in tissue samples from pulmonary hypertension patients. Soni Savai Pullamsetti, head of the research project, says, “In these patients, FoxO1 is not sufficiently active, so that the activity of various genes is not properly controlled.” As the experiments on rats and cell cultures confirmed the results, lead author of the study Rajkumar Savai explains, “If we switch off FoxO1 by means of genetic or pharmacological intervention, the vascular wall cells divide more frequently.”

The Max-Planck-Gesellschaft news release notes that reduced FoxO1 activity is therefore an important factor in the development of pulmonary hypertension. Additional experiments found that certain growth factors and chemical messengers are responsible for reduced Fox01 activity, and these are substances that are either generally associated with inflammatory processes or that stimulate cell division.

Werner Seeger, MD, says, “A potential new form of therapy could focus on increasing the activity of FoxO1 in the pulmonary arteries of patients,” which has already been demonstrated in experimental studies. Accordingly, pathological cell division in pulmonary vessel walls normalized when the researchers boosted FoxO1 activity, as indicated on the Max-Planck-Gesellschaft news release.

Seeger says, “Rats suffering from pulmonary hypertension were essentially cured.” Based on the results, the scientists are optimistic that the findings can be used to develop a new therapeutic approach for pulmonary hypertension.

Source: Max-Planck-Gesellschaft