At four weeks old, a human embryo already boasts extensive blood vessels, and by adulthood, an individual’s body contains over 60,000 miles of blood vessels—more than twice the Earth’s circumference. This intricate network ensures the supply of oxygen and nutrients to tissues, maintaining the health of organs, including the heart.

During embryonic development, specialized cells form the blood vessel lining, and additional cells contribute to the layers of the blood vessel. The vessels gradually form throughout the body and eventually merge to create the entire circulatory system. While the process slows in adulthood, the ability to grow new blood vessels persists, aiding in healing after injuries and offering potential treatments for various conditions.

In situations where a specific body part requires a new blood supply, nearby blood vessels undergo a process initiated by endothelial cells—the cells forming the blood vessel lining. These cells multiply, transforming into shape-shifters. Instead of forming a flat, tightly bound structure, they create a line that moves to the needed location. Upon reaching the destination, the cells revert to a tunnel-like structure, forming the new blood vessel.

Professor Harry Mellor and his team are researching this intricate process. Vascular endothelial growth factor (VEGF) is known to play a vital role, and attempts to stimulate new blood vessel growth through VEGF injections have been made. However, Professor Mellor notes that the process is more complex than initially thought. The team focuses on understanding cell shape changes and movements, particularly in the cytoskeleton—the cell’s framework.

With funding from the British Heart Foundation (BHF), the team has identified the role of two proteins enabling cell shape changes. Collaborating with international partners, they delve deeper into studying one of these proteins, FMNL3, aiming to enhance the understanding of the intricate processes involved in blood vessel formation