Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

A new study from the Department of Physiology, Anatomy & Genetics (DPAG) has shed light on a key regulatory step in the initiation and progression of Abdominal Aortic Aneurysm by revealing the protective role of a previously little known small protein.

Smooth muscle cell with LRP1/PDGRb trafficking through different subcellular compartments
Smooth muscle cell with LRP1/PDGRb trafficking through different subcellular compartments

An abdominal aortic aneurysm (AAA) is a bulging of the aorta, the body’s main blood vessel, which runs from the heart down through the chest and stomach. Prevalence of AAA in the population is high, up to nearly 13% depending on age group, particularly for men aged 65 and over. An AAA can get bigger over time and rupture, causing life-threatening bleeding. There is a high mortality rate of around 80% in patients with ruptured AAA; only dropping to around 50% when patients undergo surgery.  

While clinicians can monitor the beginnings of AAA, a rupture can occur suddenly without warning. Currently, the only available intervention involves a high-risk surgical procedure, which is only undertaken if there is a real danger of rupture. There are no pharmacological treatment options because the underlying causes of AAA are not fully understood.   

Scientists know that in some patients there is a genetic predisposition to AAA, and large genomic studies have identified that mutations in a large protein called LRP1 predispose people to aortic aneurysm, as well as other major vascular diseases. However, the mechanism responsible for how these mutated genes cause the disease has so far been unknown. A new paper from DPAG's Smart Group has for the first time demonstrated that a smaller protein called Thymosin β4 (Tβ4) interacts with LRP1 and is ultimately responsible for the behaviour of the smooth muscle cells of the aorta.

Read the full story on the Department of Physiology, Anatomy & Genetics website.

The story is also covered in an Oxford Science Blog

Similar stories

New small molecule found to suppress the evolution of antibiotic resistance in bacteria

Researchers from the Ineos Oxford Institute for antimicrobial research (IOI) and the Department of Pharmacology at Oxford University, have developed a new small molecule that can suppress the evolution of antibiotic resistance in bacteria and make resistant bacteria more susceptible to antibiotics.