{"id":674,"date":"2011-04-28T21:19:33","date_gmt":"2011-04-28T20:19:33","guid":{"rendered":"https:\/\/blogs.bmj.com\/heart-journalscan\/?p=674"},"modified":"2015-11-12T15:33:36","modified_gmt":"2015-11-12T14:33:36","slug":"impaired-monocyte-recruitment-leads-to-plaque-stabilisation","status":"publish","type":"post","link":"https:\/\/blogs.bmj.com\/heart\/2011\/04\/28\/impaired-monocyte-recruitment-leads-to-plaque-stabilisation\/","title":{"rendered":"Impaired monocyte recruitment leads to plaque stabilisation"},"content":{"rendered":"
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Recruitment of monocytes into atherosclerotic plaque has been shown to drive disease progression, and the presence of a higher number of macrophages has been associated with increased plaque vulnerability. \u00a0Conversely, a reduction in plaque macrophage content has been associated with plaque stabilisation; however, it has not previously been described exactly how macrophages are \u00a0removed from plaques, for example in the context of statin therapy.<\/p>\n

<\/p>\n

Potteaux et al. aimed to elucidate this mechanism by use of the mouse\u00a0Apoe-\/-\u00a0model, which has high levels of cholesterol and therefore spontaneously develops atherosclerotic lesions. \u00a0However, in this case the authors re-introduced the apoE gene (by means of an adenoviral vector), and studied what happened to the mice’s atherosclerotic plaques subsequently.<\/p>\n

Within two days of apoE complementation, plasma cholesterol levels had returned to normal levels, and HDL cholesterol levels had increased four fold, leading to a stabilisation of plaque area. \u00a0At four weeks, plaque macrophage content was noted to be 72% lower, however no egress of macrophages from plaque was noted. \u00a0Rather, the authors noted that decreased monocyte recruitment, coupled with apoptosis of existing cells, led to the reduction in plaque macrophages.<\/p>\n

Conclusions:<\/p>\n

In this mouse model, plaque stabilisation was seen to occur as a result of a decrease in monocyte recruitment, rather than an increase in macrophage egress. \u00a0Therapies to inhibit monocyte recruitment may therefore be beneficial in stabilising plaque.<\/p>\n