Abstract

Medicine![Figure][1] CREDIT: NEPHRON/WIKIMEDIA The introduction of drugs that lower serum levels of “bad” (LDL) cholesterol has had a major impact in reducing the prevalence of cardiovascular disease. By contrast, complementary efforts to harness the apparent beneficial effects of “good” (HDL) cholesterol by pharmacologically boosting serum levels of HDL have faltered. To date, such drugs have yielded disappointing results in clinical trials, which has contributed to the growing view that the abundance of HDL in serum may be less important than its biological activity. Supporting the notion that measures of HDL function are clinically relevant, Besler et al. found that HDL from healthy individuals and HDL from patients with coronary artery disease differ in their capacity to induce critical signaling events in the endothelium, the cells lining the interior of blood vessels. HDL normally stimulates nitric oxide synthesis and endothelial repair, but the HDL from the patients inhibited these processes—possibly because of the disease-associated loss of an HDL-associated enzyme, paraoxonase. Further research on the biological functions of HDL will be required to ascertain which are most critical to its protective effects against cardiovascular disease and how best to intervene therapeutically. J. Clin. Invest. 10.1172/JCI42946 (2011). [1]: pending:yes

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