Scientists are depicting a novel scheme for atherosclerosis development, suggesting that this pathology might result from an imbalance between pro-inflammatory processes and calming ones. This is one of intriguing scientific results that emerge from the Second European Vascular Genomics Network Conference (EVGN Conference - Hamburg, September 27th - 30th 2005). These results provide new insights into the role of inflammation in heart disease and led to development of new informative models of blood clot formation and the processes that lead to heart attacks.
The inflammatory process is a sort of alarm bell that indicates the onset of atherosclerosis. In the recent past it had become clear that both innate and acquired immune responses mediated by white blood cells (inflammation) play a critical role in the development of this pathology. By altering tissue homeostasis (i.e. the whole of the metabolic events that maintain internal equilibrium) the inflammatory process paves the way towards the deposition of early fatty streaks. This event in turn stimulates endothelial activation (the endothelium is the inner lining of blood vessels) favouring the recruitment of infiltrating blood cells.
But what seemed quite a chaotic process turned out to be more organized than previously envisaged. Recently, Alain Tedgui, EVGN scientific coordinator (INSERM (Institut National de la Santé et de la Recherche Médicale, Paris, France) and colleagues have provided evidence that the immuno-inflammatory responses are tightly modulated: among the actors there are two anti-inflammatory cytokines that counter-balance the effects of other pro-inflammatory mediators.
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