This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. In general HDL (the """"""""good cholesterol"""""""") is inversely correlated for risk for coronary artery disease (i.e. the more HDL a person has, the less likely it is that the person will have coronary artery disease). However, while this is true for populations, in fact about 40 to 45% of all heart attacks occur in subjects with perfectly normal HDL levels. Our preliminary research has shown that HDL from normal individuals (.i.e those without known coronary artery diseas) is able to inhibit lipid oxidation and is ant-inflammatory. In contrast, we have found in this preliminary research that individuals with normal HDL-cholesterol levels who have coronary artery disease almost always have HDL that is dysfunctional. Their HDL is less able to inhibit lipid oxidation and in fact may actually promote lipid oxidation and instead of being anti-inflammatory, their HDL is pro-inflammatory.
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