Medical discovery 'first step' to new painkillers
A major medical discovery by UK scientists could lead to the development of an entirely new type of painkiller.
A drug resulting from the research, published in the journal Neurobiology of Disease, would offer new hope to sufferers of chronic pain conditions such as traumatic nerve injury, for which few effective painkillers are currently available.
The work focuses on a signal protein called vascular endothelial growth factor (VEGF).
VEGF controls the re-growth of blood vessels in tissues which have been damaged by injury. It is a widely targeted compound for cancer, eye disease and other illnesses in which abnormal blood vessel growth occurs.
Drugs are used to inhibit the VEGF in cancer, which can otherwise lead to the formation of new blood vessels that provide oxygen and nutrients to tumours.
Lead researcher Professor Alan Bates and colleagues had previously discovered in 2002 that VEGF comes in two forms and acts like a switch – one which turns on the growth of blood vessels and another that blocks growth.
However, this latest research has shown for the first time that these two forms of VEGF not only act on blood vessels but also differently affect the sensory nerves that control pain.
The academics discovered that the VEGF that promotes blood vessel growth causes pain, while the other, which inhibits blood vessel growth, prevents pain.
The study has centred on understanding how these two types of VEGF work and why the body makes one form rather than the other.
The academics have been able to switch from the pain stimulating form to the pain inhibiting VEGF in animal models in the laboratory and are now investigating compounds to replicate this in humans. It is thought these compounds could form the basis for new drugs to be tested in humans in clinical trials.
The work has been led by Dr Lucy Donaldson in The University of Nottinghams's School of Life Sciences, in collaboration with Professor Bates, Professor of Oncology in the University's Cancer Biology Unit.