Platelets are central players in the development of atherothrombosis. As such, anti-platelet therapies remain a cornerstone for the treatment of cardiovascular disease. However, current anti-platelet approaches are often limited by their propensity to cause bleeding complications. Moreover, in certain conditions, such as diabetes, patients may exhibit a hyperactive platelet phenotype that is relatively resistant to standard anti-platelets. Recent experimental evidence has now emerged demonstrating that the processes underpinning platelet activation, and in vivo thrombosis formation, are more complex that previously recognised. This has led to the exciting possibility of developing novel anti-platelet strategies that can inhibit thrombosis whilst sparing haemostasis.
In addition to their role mediating atherothrombosis, there is now a large body of evidence that platelets have essential immune and inflammatory function. As such, platelets are now implicated in a range of clinical conditions including autoimmune diseases, sepsis, cancer and ischaemia-reperfusion injury.
The critical role of platelets in atherothrombosis, inflammation, immunity and cancer has spurred significant interest to discover novel approaches to inhibit platelet function given the broad relevance to both cardiovascular and inflammatory diseases. An important aspect of this quest for novel anti-platelet approaches is understanding the multiple biochemical and biophysical signals that can lead to platelet activation. Indeed, deciphering the precise mechanisms that govern platelet reactivity and activation are likely to key to uncovering new anti-platelet approaches that can inhibit platelet function whilst sparing haemostasis.
This research topic will accept Original Research, Opinions, Perspectives and Reviews on platelet biology, in particular:
1) Novel anti-platelet drugs.
2) Novel regulators of platelet function.
3) Role of mechanobiology in regulating platelet function.
4) Role of platelets in immune and inflammatory diseases.
5) 'omics' and platelet function.
Platelets are central players in the development of atherothrombosis. As such, anti-platelet therapies remain a cornerstone for the treatment of cardiovascular disease. However, current anti-platelet approaches are often limited by their propensity to cause bleeding complications. Moreover, in certain conditions, such as diabetes, patients may exhibit a hyperactive platelet phenotype that is relatively resistant to standard anti-platelets. Recent experimental evidence has now emerged demonstrating that the processes underpinning platelet activation, and in vivo thrombosis formation, are more complex that previously recognised. This has led to the exciting possibility of developing novel anti-platelet strategies that can inhibit thrombosis whilst sparing haemostasis.
In addition to their role mediating atherothrombosis, there is now a large body of evidence that platelets have essential immune and inflammatory function. As such, platelets are now implicated in a range of clinical conditions including autoimmune diseases, sepsis, cancer and ischaemia-reperfusion injury.
The critical role of platelets in atherothrombosis, inflammation, immunity and cancer has spurred significant interest to discover novel approaches to inhibit platelet function given the broad relevance to both cardiovascular and inflammatory diseases. An important aspect of this quest for novel anti-platelet approaches is understanding the multiple biochemical and biophysical signals that can lead to platelet activation. Indeed, deciphering the precise mechanisms that govern platelet reactivity and activation are likely to key to uncovering new anti-platelet approaches that can inhibit platelet function whilst sparing haemostasis.
This research topic will accept Original Research, Opinions, Perspectives and Reviews on platelet biology, in particular:
1) Novel anti-platelet drugs.
2) Novel regulators of platelet function.
3) Role of mechanobiology in regulating platelet function.
4) Role of platelets in immune and inflammatory diseases.
5) 'omics' and platelet function.
