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MHH molecular biologist investigates the body's own repair programme in the heart muscle and receives the renowned ERC Advanced Grant from the European Union
When someone suffers a myocardial infarction, heart muscle cells die. The body then launches a healing programme: cells of the immune system trigger an inflammatory response in the heart muscle that breaks down the dead tissue. At the same time, fibroblasts are activated, which form connective tissue cells and replace the damaged heart muscle tissue. Scar tissue thus forms at the site of the injury. The interplay between inflammation and fibroblast activation is complex and determines whether the heart can be repaired properly after a heart attack or not. If the tissue becomes too scarred, fibrosis occurs and the heart muscle stiffens. This reduces its pumping action and can lead to heart failure. Targeted therapeutic approaches to influence these processes have not yet been clinically implemented. Experts assume that the repair processes in the heart vary from person to person. In addition, heart injuries and treatments also affect other organs.
In his MIGRATe project, Professor James Thackeray, a molecular medicine specialist at the Clinic for Nuclear Medicine at Hannover Medical School (MHH), wants to research non-invasive molecular imaging approaches to examine inflammatory cells and the activation of fibroblasts in the heart and in the network organs connected to it, and thus to precisely control targeted therapeutic interventions . The European Research Council (ERC) is funding the project with a Consolidator Grant for five years with around two million euros. The grants awarded by the ERC are highly regarded within the scientific community. With the Consolidator Grant, the ERC supports excellent scientists in their innovative research projects and the further expansion of their working groups.
Finding the optimal time for therapy
For seven years, the scientist has headed a research group for translational and cardiovascular molecular imaging, which is using state-of-the-art imaging techniques to gain new insights into the progression of cardiovascular diseases. ‘Standard medical therapy is unable to take into account the individual differences in the early biological processes of heart repair after a heart attack,’ says the scientist. ‘Therefore, it is currently impossible to predict whether someone will develop heart failure after the first attack or not.’ With the help of imaging, Professor Thackeray now wants to determine the optimal time and optimal alignment of treatment to support the body's own healing process and prevent the progression of heart failure. To do this, he uses certain radionuclide imaging markers, known as tracers. These tiny tracers are weakly radioactive for a short period of time and can be visualised using high-resolution positron emission tomography (PET). ‘The tracers enable us to detect and precisely determine the early processes of inflammation and fibroblast activation that contribute to cardiac remodelling and ultimately lead to organ failure,’ emphasises the molecular medicine specialist.
Heart attack also affects the brain, liver and kidneys
In terms of communication between organs, Professor Thackeray and his team are particularly interested in the heart's connection to the brain, kidneys and liver. This is because inflammation and immune system activity affect the heart-brain axis, for example, such that inflammatory cells in the heart stimulate the activation of inflammatory cells in the brain. This, in turn, can exacerbate the progression of heart failure. Heart disease is also associated with kidney and liver failure, which may be due to both increased inflammation and fibroblast activation. ‘In this project, we can measure each of our imaging markers outside the heart at the same time to determine how immune cells and fibroblasts contribute to the consequential damage to the other organs.’
However, the researchers are not relying on imaging techniques alone. They want to combine these with molecular biology methods to decode the microenvironment of the tissue. In this way, they hope to distinguish between the detrimental and beneficial cell populations that control the balance between healing and harmful inflammation and fibroblast activity, and find new biomarkers for post-heart attack treatment. In addition, PET imaging can also be used to monitor the molecular response to therapy during treatment. The aim is to identify individually which patients exhibit the molecular markers and will therefore respond to the treatments before the therapy begins. Ideally, these can then be influenced in such a way that an effective balance can be restored between the positive and healing aspects of the inflammation and fibroblast activity and the negative aspects. This should improve heart health after an acute myocardial infarction – with corresponding benefits for the brain, kidneys and liver.
SERVICE:
For further information, please contact Professor Dr James Thackeray, thackeray.james@mh-hannover.de.
Professor Dr. James Thackeray wants to improve personalised treatment after heart attack.
Copyright: Karin Kaiser/MHH
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Professor Dr. James Thackeray wants to improve personalised treatment after heart attack.
Copyright: Karin Kaiser/MHH
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