Chronic regeneration of damaged endothelial cells at sites of disturbed blood flow in the vasculature promotes the development of atherosclerosis. Now an LMU team has further elucidated the role of a short RNA molecule in atherogenesis.
Atherosclerosis – the condition popularly known as hardening of the arteries – develops almost exclusively at junctions and sharp turns in the arterial tree. This is because, at such sites, the endothelial cells that form the lining of the blood vessels are particularly sensitive to damage – and must be constantly repaired or replaced. A research team led by LMU’s Andreas Schober has now provided further evidence that a specific micro-RNA, called miR-103, can stimulate the development of atherosclerosis. Their findings appear in the journal Nature Communications.
As the blood courses through unbranched arteries, the endothelial cell layer is exposed to high shear stresses. Not only does the endothelium withstand these stresses, they are actually required to maintain the function of the cell layer. However, bifurcations or tight turns in the vasculature disturb the flow by causing turbulence, which reduces the shear force imposed on the endothelium. This in turn has deleterious consequences for the endothelial cells at such sites. “As a result, endothelial cells located at bifurcations are subjected to chronic damage and must be constantly replaced,” Schober explains. This process is accompanied by the accumulation of lipids on the inner face of the blood-vessel wall, which leads to inflammatory reactions that stimulate the formation of atherosclerotic lesions. As we get older, these lesions tend to grow, which can have life threatening repercussions.
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