The Vascular Research team is relatively new to Aston University; however it has already made a significant contribution to Aston’s research output (see here). Our research interests are primarily focused on the vascular basis of diseases, particularly in the areas of angiogenesis (how new blood vessels form from pre-existing vessels) and vascular protection.
We are committed to translational research (“from bench to bedside”) with a view to develop our discoveries from invention through to practical application, maintaining a clear focus on helping people affected by the conditions we study. Through our research we hope to understand the pathogenesis (origins) of vascular diseases such as preeclampsia and arthrosclerosis and to develop therapeutic interventions based on our findings.
The team is led by Asif Ahmed, Professor of Vascular Biology and Pro-Vice-Chancellor for Health at Aston University. Prof Ahmed has an international reputation in angiogenesis and vascular protection research and is known for producing world-leading research in his area of expertise. He is joined as part of the Vascular Aston team by Dr Shakil Ahmad, Dr Keqing Wang and Dr Meng Cai.
Our current research projects are focused particularly on preeclampsia, taking a multi-dimensional approach to evaluating potential causes of the disorder and developing new therapies based on our findings. The team has a wealth of experience between them and our collective research strategy is based on years of academic study, its direction having been influenced by a number of key discoveries along the way.
In 2000, Prof Ahmed discovered that an enzyme called placental Heme Oxygenase (HO) protects the human placenta against injury. He went on to identify carbon monoxide (CO), the gaseous product of HO, as an inhibitor of two anti-angiogenic proteins (soluble Flt-1 and soluble endoglin). Soluble Flt-1 has been increasingly recognized as a major factor responsible for the clinical signs of preeclampsia. In 2004 Ahmed & Ahmad identified soluble Flt-1 as the single most important molecule responsible for angiogenic imbalance in preeclampsia, by demonstrating that the removal of sFlt-1 from preeclamptic samples restored angiogenic balance.
In a 2007 study, Prof Ahmed’s team discovered that increasing heme oxygenase activity could provide protection against preeclampsia. This discovery has formed the basis for the world’s first randomized controlled clinical trial on the use of statins in pregnancy, the StAmP Trial, which is currently ongoing at Aston University. This trial aims to determine whether statins can be used effectively to ameliorate the symptoms of early-onset preeclampsia. If successful, it could allow serious cases of preeclampsia to be treated using drugs which are already widely available, and could be the first major step towards curing preeclampsia altogether (see here).
The Vascular Aston team recently identified another diatomic molecule, hydrogen sulfide (H2S), as offering the potential to treat both preeclampsia and fetal growth restriction in pregnancy. These findings have been published in the prestigious scientific journal Circulation and were highlighted as being “groundbreaking” both by Circulation and within the mainstream media. This is the first time two naturally-occurring small gaseous molecules (CO and H2S) have been shown to prevent the release of the culprit proteins (sFlt-1 and sEng) which are elevated in preeclampsia. More importantly, in this new work we have shown that it is possible to restore fetal growth and fix the vascular abnormalities (angiogenesis) in preeclamptic placenta by restoring hydrogen sulfide levels.
The Vascular Aston team will continue to evaluate the effects of anti-angiogenic growth factors that contribute to vascular disorders, in particular preeclampsia, and develop therapeutic targets for these conditions. The ongoing StAmP trial and our research into the effects of hydrogen sulfide are both promising avenues which we will continue to pursue, with the aim of developing novel therapies for preeclampsia. We hope that before the end of the decade our research will allow us to develop a single treatment for the condition that will change clinical approaches to managing preeclampsia for future generations.