HighDensityLipoprotein

HighDensityLipoprotein, commonly abbreviated as HDL, is one of the major classes of lipoprotein particles that transport lipids in the bloodstream. HDL particles are smaller and denser than other lipoproteins and contain apolipoproteins, notably ApoA-I and ApoA-II, along with phospholipids, cholesterol, and cholesteryl esters. In clinical practice, HDL cholesterol (HDL-C) is measured to assess this lipoprotein’s concentration in blood.

HDL is central to reverse cholesterol transport, a pathway that moves cholesterol from peripheral tissues back to the liver for excretion or reuse. Nascent HDL is formed in the liver and intestine and awakens maturation as it acquires cholesterol from cells. Lecithin–cholesterol acyltransferase (LCAT) esterifies free cholesterol, transforming HDL into mature, spherical particles. Cholesteryl ester transfer protein (CETP) can exchange cholesteryl esters and triglycerides with other lipoproteins, linking HDL metabolism to very-low-density and low-density lipoproteins. Uptake of HDL cholesterol by the liver primarily occurs via the scavenger receptor B type I (SR-BI).

Clinically, higher HDL-C levels have been associated with lower cardiovascular risk in observational studies. However, raising HDL-C pharmacologically has not consistently reduced cardiovascular events, highlighting that HDL’s protective effects depend on function as well as quantity. HDL possesses anti-inflammatory, antioxidative, and antithrombotic properties and can support endothelial health. Researchers also assess HDL function, such as cholesterol efflux capacity, as a complementary indicator beyond HDL-C.

HDL function can be altered by inflammation or oxidative stress, and under certain conditions HDL may become dysfunctional or pro-inflammatory. Genetic factors can also influence HDL metabolism and function, contributing to individual variation in cardiovascular risk.