MADRID, 30 (EUROPA PRESS)
Researchers at the Max Planck Institute for Molecular Biomedicine and of the Westphalian Wilhelms-University in Münster, Germany, have described a regulatory mechanism key in controlling the growth of blood vessels that can help to solve problems of resistance to drugs in the future.
Angiogenesis, the growth of new blood vessels, is a complex process during which different signaling proteins interact with each other in a coordinated model. In this process, the growth factor VEGF signaling pathway ' Notch ' play important roles.
In particular, VEGF promotes the growth of vessels holding to its receptor (VEGFR2) and ' Notch ' acts as a switch capable of suppressing angiogenesis. Until recently, scientists thought that ' Notch ' deleted the effects of VEGF through regulation of VEGFR2 downward.
Researchers have shown that a defective signalling ' Notch ' allows that strong, uncontrolled vessel, growth occurs even when VEGF and VEGFR2 are inhibited. In this case, a different family VEGFR3, VEGF receptor, is heavily regulated to high, which promotes angiogenesis.
According to the CEO of MPI and head of the Department of tissue biology and Morphogenesis, Ralf Adams, “this finding may help explain the resistance to drugs in certain types of cancer therapies and can become the basis of new treatment strategies”.
An extensive ramified network of blood vessels provides nutrients to every organ of the body and removes the metabolic waste products from the tissues. The growth of this vascular system is essential for the development and the process of wound healing.
Uncontrolled angiogenesis contributes to the emergence of diseases such as hemangiomas or retinopathy that damage the vision of people with diabetes and the elderly. Inhibition of angiogenesis in cancer therapy, is used to kill of ' hunger ' tumors and preventing their metastasis through circulation.
Currently, this often become directed against VEGF or its receptor VEGFR2. When his supply of oxygen becomes inappropriate, begin to liberate VEGF, who joins VEGFR2, activating the receptor and thus activating the vessel growth.
Thus, the formation of new blood vessels can block by inhibiting VEGF or VEGFR2. Unfortunately, existing treatments are inadequate and, for reasons unknown, some patients respond poorly or do not respond to VEGF/VEGFR2 inhibition.
According to Adams, “what we need to do now is to confirm if VEGFR3 and other regulated by Notch signals are, in fact, capable of promoting the growth of independent of VEGF vessels in eye disease or cancer, not only in mice, also in humans”.
“Might be possible as well predict if patients, depending on their status of activation of ' Notch ' vascular, will respond to inhibition of VEGF or VEGFR2.” “This would allow doctors to choose alternative therapies, if necessary”, he concludes.
