Translation of "Neoangiogenesis" in German

This phenomenon is referred to as neoangiogenesis (“in-grown vessels”).

Sunitinib inhibits multiple receptor tyrosine kinases (RTKs) that are implicated in tumour growth, neoangiogenesis, and metastatic progression of cancer.

This breakdown leads to a significant loss of the biological activity and may thus, despite the increased expression of the VEGF receptors, underlie a deficient stimulation of neoangiogenesis in the chronic wound environment.

In preclinical studies, regorafenib has been shown to inhibit several angiogenic VEGF receptor tyrosine kinases that play a role in tumor neoangiogenesis (the growth of new blood vessels).

These are e.g., benign or malignant tumors, particularly tumors of epithelial and neuroepithelial origin, metastasization and the abnormal proliferation of vascular endothelial cells (neoangiogenesis).

In preclinical studies, regorafenib inhibits several angiogenic VEGF receptor tyrosine kinases that play a role in tumor neoangiogenesis (the growth of new blood vessels).

Neoangiogenesis is required in particular for maintaining expansive tumor growth, since only sufficient oxygenation will ensure the supply with nutrients to and removal of tumor degradation products from the tumor.

This growth is associated with numerous changes in the environment of the malignant cells, including neoangiogenesis, to ensure a supply of nutrients and oxygen and others to the malignant tumor.

Moreover, growth factors and, in particular, BMP-2, BMP-7, and proteins derived from them, neoangiogenesis-inducing proteins, steroid hormones, bisphosphonates, and antiphlogistics can be used.

Composite material according to claim 7, wherein the antiseptic is selected from the group consisting of chlorhexidine, octenidine, dequalinium chloride, polyhexanide, oligomeric biguanides, BMP-2, BMP-7, and proteins derived from them, neoangiogenesis-inducing proteins, steroid hormones, bisphosphonates, and antiphlogistics.

While the blood is passing through the vessels, the endothelium basically is acted upon not only by shearing forces but, naturally, also by the initially mentioned pressures, whereby a pressure increase lasting for as long as possible will, in principle, lead to an increased release of vessel-forming genes (VEGF genes, vascular endothelial growth factor encoding genes), which will be beneficial to the regeneration of the heart vessels and, in particular, neoangiogenesis.

SUMMARY The invention now aims to enhance the contribution to neoangiogenesis based on a pressure increase or changing pressure sensitivity and to improve these effects theoretically recognized as positive.

It could be experimentally demonstrated that a linear pressure increase as well as the mere shearing stress of the endothelium contribute considerably less to the production of vascular endothelial growth factors, and hence to neoangiogenesis.

During the occlusion, i.e. with the balloon 10 inflated, pressure medium is thus pulsingly introduced into the vibrator body 13 via lumen 14 so as to obtain the respective pressure change load by the thus enhanced stimulation of the factors triggering neoangiogenesis.

SUMMARY OF THE INVENTION The invention now aims to enhance the contribution to neoangiogenesis based on a pressure increase or changing pressure sensitivity and to improve these effects theoretically recognized as positive.

The compounds of the invention can additionally be employed therapeutically in the control of neoplastic disorders, especially those disorders characterized by metastasis associated with neoangiogenesis.

In that case, tumour patients experience a healing effect, since the growth of the tumour is blocked by preventing the proliferation of endothelial cells and hence by avoiding neoangiogenesis.

Prior experimental examinations suggested that the improvement in the ventricular function following experimentally induced myocardial infarction is due to a stimulated neoangiogenesis which leads to late myocardial remodelling by increased myocardial bloodflow, rescue of resting myocardium, the reduction of the myocardial fibrosis and the reduced apoptosis of hypertrophic myocytes in the peri-infarction region (Kawamoto A, Gwon H C, Iwaguro H, Yamaguchi J l, Uchida S, Masuda H, Silver M, Ma H, Kearney M, Isner J M, Asahara T. Therapeutic potential of ex vivo expanded endothelial progenitor cells for myocardial ischemia.

These are, for example, benign or malignant tumours, in particular tumours of epithelial and neuroepithelial origin, formation of metastases and the abnormal proliferation of vascular endothelial cells (neoangiogenesis).

At the RTC we were able to demonstrate in studies with mice that an intramyocardial application of bone marrow- and umbilical blood-derived cells after ischemic damage had a positive effect on the neoangiogenesis and the survival of the animal in a myocardial infarction model.

In combination with conventional therapies such as chemo- and radiotherapy, prevention of pathological neoangiogenesis, commonly occurring in malignant growths, is a promising approach to treating tumours.

In preclinical studies, Stivarga inhibits several angiogenic VEGF receptor tyrosine kinases that play a role in tumor neoangiogenesis (the growth of new blood vessels).