AI Article Synopsis
- Monocyte-macrophages (MoMas) are essential in the development of atherosclerosis, and their behavior in humans was analyzed in different groups: familial hypercholesterolemia (FH), non-familial hypercholesterolemia (NFH), and normocholesterolemic (CTRL) patients.
- The study found that both FH and NFH patients had higher levels of pro-inflammatory M1 MoMas compared to CTRL, while anti-inflammatory M2 MoMas were decreased, especially in NFH.
- A significant correlation was identified between LDL cholesterol levels and the presence of atherosclerotic plaques, suggesting that human hypercholesterolemia leads to an imbalance in monocyte populations that may increase atheros
Article Abstract
Monocyte-macrophages (MoMas) play a major role in atherosclerosis. In mice, hypercholesterolemia increases pro-inflammatory monocytes that promote plaque growth, but whether this is true also in humans in unknown. We herein analyzed monocyte subsets and MoMa phenotypes in familiar (FH, n = 22) and non-familiar (NFH, n = 20) hypercholesterolemic compared with normocholesterolemic (CTRL, n = 20) patients. We found that FH and NFH had higher circulating pro-inflammatory CD68(+)CCR2(+) M1 MoMas than CTRL, while anti-inflammatory CX3CR1(+)CD163(+)/CD206(+) M2 MoMas were reduced only in NFH. As a result, the M1/M2 polarization balance was increased in FH and, more markedly in NFH. M1 MoMas and the M1/M2 polarization ratio were directly correlated to pre-treatment LDL cholesterol levels and strongly associated with the presence of atherosclerotic plaques. In conclusion, we show for the first time that human hypercholesterolemia is associated with a pro-inflammatory imbalance of circulating monocytic cells, which can predispose to the development of atherosclerosis.
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| http://dx.doi.org/10.1016/j.atherosclerosis.2014.10.106 | DOI Listing |
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