Journal
CLINICAL CHEMISTRY
Volume 67, Issue 1, Pages 183-196Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/clinchem/hvaa296
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Funding
- National Institutes of Health [5T32HL007575-33]
- Kowa Research Institute
- Kowa Pharmaceuticals Europe Co. Ltd
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This review focuses on the role of triglyceride-rich lipoprotein (TRL) remnants in atherosclerosis, highlighting key metabolic mechanisms and assay methods. Multiple lines of evidence suggest that TRL remnants play a central role in residual cardiovascular risk.
BACKGROUND: Triglycerides, cholesterol, and their metabolism are linked due to shared packaging and transport within circulating lipoprotein particles. While a case for a causal role of cholesterol-carrying low-density lipoproteins (LDLs) in atherosclerosis is well made, the body of scientific evidence for a causal role of triglyceride-rich lipoproteins (TRLs) is rapidly growing, with multiple lines of evidence (old and new) providing robust support. CONTENT: This review will discuss current perspectives and accumulated evidence that an overabundance of remnant lipoproteins stemming from intravascular remodeling of nascent TRLs-chylomicrons and very low-density lipoproteins (VLDL)-results in a proatherogenic milieu that augments cardiovascular risk. Basic mechanisms of TRL metabolism and clearance will be summarized, assay methods reviewed, and pivotal clinical studies highlighted. SUMMARY: Remnant lipoproteins are rendered highly atherogenic by their high cholesterol content, altered apolipoprotein composition, and physicochemical properties. The aggregate findings from multiple lines of evidence suggest that TRL remnants play a central role in residual cardiovascular risk.
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