6533b7d8fe1ef96bd1269b4a
RESEARCH PRODUCT
Initiation and progression of atherosclerosis – enzymatic or oxidative modification of low-density lipoprotein?
Karl J. LacknerMichael Torzewskisubject
medicine.medical_specialtyLipoprotein modificationHydrolasesClinical BiochemistryOxidative phosphorylationDiseaseModels Biologicalchemistry.chemical_compoundInternal medicinemedicineAnimalsHumansMacrophagechemistry.chemical_classificationVascular diseaseBiochemistry (medical)General MedicineSterol EsteraseAtherosclerosismedicine.diseaseLipoproteins LDLC-Reactive ProteinEndocrinologyEnzymechemistryLow-density lipoproteinlipids (amino acids peptides and proteins)Oxidation-ReductionPeptide HydrolasesLipoproteindescription
AbstractAtherosclerosis is widely regarded as a chronic inflammatory disease that develops as a consequence of entrapment of low-density lipoprotein (LDL) in the arterial intima. Native LDL lacks inflammatory properties, so the lipoprotein must undergo biochemical alterations to become atherogenic. Among several other candidates, two different concepts of lipoprotein modification are propagated, the widespread oxidation hypothesis and the less common E-LDL hypothesis, which proposes that modification of LDL occurs through the action of ubiquitous hydrolytic enzymes (enzymatically modified LDL or E-LDL) rather than oxidation. By clearly distinguishing between the initiation and progression of atherosclerotic lesion development, this article reviews comparative studies of both types of lipoprotein modification and submits a viewpoint for discussion proposing that these lipoprotein modifications do not really compete, but rather complement one another. According to this concept, E-LDL might be more important for the initiation of atherosclerosis, while oxidative modification of LDL might be more helpful for diagnosis and prognosis of the disease.Clin Chem Lab Med 2006;44:1389–94.
year | journal | country | edition | language |
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2006-12-14 | Clinical Chemistry and Laboratory Medicine (CCLM) |