High‐density lipoprotein: A potent inhibitor of inflammation

Abstract

1. Inflammation is an important process, driving the progression of atherosclerosis. Stemming inflammation may be a mechanism to inhibit the progression of this disease. 2. High-density lipoprotein (HDL), a particle inversely related to cardiovascular disease, has been described as having a number of anti-inflammatory functions. It has been shown that HDL inhibits endothelial inflammation in both in vitro and in vivo models, reducing the expression of key cell adhesion molecules. In addition, HDL has been shown to have an effect on the coagulation pathway by inhibiting platelet activation and reducing thrombus formation. Furthermore, by reducing the activation of leucocytes, HDL can inhibit leucocyte recruitment to the endothelium. 3. High-density lipoprotein infusion studies conducted in patients with inflammatory diseases have shown that acute treatment with HDL can effectively inhibit inflammation in vivo. Thus, HDL has been proven to be a potent inhibitor of inflammation, acting on a number of pathways, and this may suggest that HDL could be applied as an anti-inflammatory molecule for a number of diseases. 4. The present review highlights these important studies and reviews data on the anti-inflammatory effects of HDL from in vitro and in vivo studies, in both humans and animal models of atherosclerosis and inflammatory-related diseases.

Hypercholesterolaemia, signs of islet microangiopathy and altered angiogenesis precede onset of type 2 diabetes in the Goto–Kakizaki (GK) rat

“…ESM Table 3 shows that systemic HDL-cholesterol levels and total cholesterol/HDL-cholesterol ratio correlated negatively and positively, respectively, with pancreas/islet expression of Casp1, IL18 and IL15. These data are in agreement with the well-recognised antiinflammatory effects of HDL [38].…”

Mild Hypercholesterolemia Blunts the Proinflammatory and Prothrombotic Effects of Hypertension on the Cerebral Microcirculation

“…These findings are consistent with reports describing an antiinflammatory action of HDL cholesterol, [31][32][33] genetic overexpression of ApoA1 34,35 as well as 4F treatment. 36,37 The antiinflammatory effects of HDL and ApoA1 have been attributed to an attenuation of leukocyte activation 38 and endothelial cell adhesion molecule expression, 39 possibly resulting from enhanced nitric oxide production. 40 High-density lipoprotein also appears to exert antiplatelet effects, including inhibition of agonist induced platelet aggregation, fibrinogen binding, granule secretion, and production of thromboxane A2.…”

Monocyte to high-density lipoprotein cholesterol ratio is predictive of in-hospital and five-year mortality in ST-segment elevation myocardial infarction

“…First, HDL-C prevents monocyte recruitment into the artery wall by inhibiting the expression of endothelial adhesion molecules [17]. In addition, HDL-C has a role in control of the monocyte activation and proliferation of monocyte progenitor cells [18][19][20]. Furthermore, HDL-C inhibits oxidation of LDL-C and promotes efflux of oxidized LDL-C from foam cells [5,18].…”