The damages from heart attacks and stroke could be radically reduced by a simple injection, according to a new study.
Researchers at the University of Leicester are developing a simple injection to limit the devastating consequences of heart attacks and strokes.
Described by the lead researcher as “a fascinating new achievement”, work has already begun to translate the research into novel clinical therapies.
Prof Wilhelm Schwaeble of the Department of Infection, Immunity and Inflammation at the University of Leicester and collaborators identified an enzyme, Mannan Binding Lectin-Associated Serine Protease-2 (MASP-2) that is found in blood and is a key component of the lectin pathway of complement activation, a component of the innate immune system.
The lectin pathway is responsible for the potentially devastating inflammatory tissue response that can occur when any bodily tissue or organ is reconnected to blood supply following ischaemia – a temporary loss of that blood supply and the oxygen that it carries.
This excessive inflammatory response is, in part, responsible for the morbidity and mortality associated with myocardial infarction (heart attack) and cerebrovascular accidents (CVAs or strokes). Moreover, the work succeeded in finding a way to neutralise this enzyme by raising a therapeutic antibody against it.
A single antibody injection in animals has been shown to be sufficient to disrupt the molecular process that leads to tissue and organ destruction following ischaemic events, resulting in significantly less damage and markedly improved outcomes.
“This is a fascinating new achievement in the search for novel treatments to significantly reduce the tissue damage and impaired organ function that occur following ischaemia in widespread and serious conditions such as heart attacks and strokes,” said Schwaeble.
“This new potential therapy was also shown in animals to significantly improve outcomes of transplant surgery and may be applicable to any surgical procedure where tissue viability is at risk due to temporary interruption of blood flow.
“The main focus of our work was to identify a key molecular mechanism responsible for the overshooting inflammatory response that can cause substantial destruction to tissues and organs following their temporary loss of blood supply, a pathophysiological phenomenon called ischaemia/reperfusion injury,” said Schwaeble.
“Limiting this inflammatory response in oxygen-deprived tissues could dramatically improve outcomes and survival in patients suffering heart attacks or strokes,” he added.
The study has been published in the Early Online Edition of the Proceedings of the National Academy of Sciences.