How can we use the molecule cAMP to repair damaged blood vessels?

Mechanisms underlying the vascular protective effects of cAMP: Actin cytoskeleton remodelling and MKL-dependent gene expression

Dr Mark Bond at the University of Bristol has been awarded a PhD studentship to look at how a molecule called cyclic adenosine 3’, 5’-monophosphate (cAMP) could be used to develop new treatments for people with vascular diseases such as atherosclerosis. In a healthy person, cAMP signalling helps protect blood vessels from injury. It does so by regulating the survival, death and movement of cells in the vessel walls. The student will be looking at the molecules which cAMP interacts with, in particular actin, which is key to the structure of cells. Atherosclerosis is the build-up of fatty materials in the walls of the vessels. It commonly leads to coronary heart disease, the leading cause of death worldwide, which involves narrowing of the vessels supplying the heart with oxygen-rich blood. Despite improvements in treatment, progress is still yet to be made. By gaining a deeper understanding of the actions of cAMP, the researchers hope to learn how to exploit its protective effects and repair the vessel damage caused by vascular diseases such as atherosclerosis.