Plaque vulnerability in atherosclerosis: Driven by interplay between co-stimulatory signalling and extracellular matrix?
The integriity of the extracellular matrix (ECM) - the dynamic structures making up the microenvironment around cells - is of crucial impostance for the development and stability of atherosclerotic plaques. Key players in modulating inflammatory reactions in such lesions are the co-stimulatory molecules that direct the actions of immune cells. I believe that the co-stimulatory molecules are a key link between inflammation and the ECM milieu, allowing interactions between immune cells and plaque ECM to be the driving force behind atherosclerotic plaque destabilization. The aim of my research is to define how atherosclerotic plaque progression is driven via co-stimulatory molecules´ effeccts on ECMintegrity, and my ultimate goal is to identify new drug targets and strategies to promote plaque stability.
To reach my goal I am analysing both human and mouse plaques to identify
- co-stimulatory molecules expression patterns in plaques
- how interplay between co-stimulatory molecules and ECM components in plaques affects plaque vulnerability, and
- the specific molelcular mechanisms that link co-stimulatory signalling and ECM turnover.
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