The CRP and endothelial cell damage of coronary arteries

C-reactive protein induced human coronary artery endothelial cells damage.
Cardiovascular disease (CVD) is a key contributor to the global burden of disease. It is responsible for about 30% of all deaths. The mounting evidence has suggested that atherosclerosis is a major cause of CVD and a predictor of impending cardiovascular events and postcardiac outcomes. Atherosclerosis is a complex chronic disease related with a variety of risk factors, which play an important role in endothelial cell injury.
Many studies were conducted to investigate the association between endothelium damage and subclinical atherosclerosis in general population. Previous studies have showed the roles of C-reactive protein (CRP) in atherosclerosis but the underlying mechanisms are still unclear.
The group of researchers from The First Affiliated Hospital of Anhui Medical University studied the effect of C-reactive protein (pentameric CRP and monomeric CRP) on the function of endothelial cells of the coronary arteries. Furthermore, they investigated a new mechanism for regulating gene expression. This is something that the researchers are starting to explore more nowadays.
The results of their study, published in the journal BJBMS suggested that the key role of p38 MAPK in C-reactive protein (p/m) induced-cell injury. This provides a new therapy for the injury of human coronary artery endothelial cells in atherosclerosis. Hopefully with further research we can perfect the theory construction for this circulating biomarker associated with atherosclerosis.

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Editor: Edna Skopljak

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