HDL function as a target of lipid-modifying therapy.
High-density lipoprotein (HDL) is conventionally believed to possess many features that protect against atherosclerosis. However, these lipoproteins may be modified in certain individuals and/or circumstances to become pro-inflammatory. The ability of HDL to inhibit or paradoxically to enhance vascular inflammation, lipid oxidation, plaque growth, and thrombosis reflects changes in specific enzyme and protein components. The anti-inflammatory and pro-inflammatory functional properties of HDL can now be assessed using cell-based and cell-free assays. Acute or chronic systemic inflammation and the metabolic syndrome appear to render HDL pro-inflammatory. In contrast, statins and experimental agents such as apolipoprotein A-1 mimetics render HDL more anti-inflammatory. The 2 main classes of existing drugs for HDL modification are fibric acid derivatives, also known as "fibrates," and niacin- containing compounds. In several controlled and prospective intervention studies, patients with low HDL-C and additional risk factors benefited from treatment with fibrates or niacin. However, an increase in HDL-C did not lead to a decrease in cardiovascular events in all trials.
Watson
Karol E
KE
Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.
Ansell
Benjamin J
BJ
Watson
Andrew D
AD
Fonarow
Gregg C
GC
D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy* / Q000473:pathology; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007249:Inflammation / Q000097:blood / Q000473:pathology / Q000517:prevention & control; D008075:Lipoproteins, HDL / Q000097:blood* / Q000187:drug effects; D016896:Treatment Outcome
D000960:Hypolipidemic Agents; D008075:Lipoproteins, HDL