HDL and Reverse Cholesterol Transport.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic reasoning and existing literature without original human data or systematic review methodology.
PubMed 31071007 · doi:10.1161/CIRCRESAHA.119.312617
What was done
The authors reviewed the biological mechanisms of high-density lipoprotein (HDL) in reverse cholesterol transport (RCT). They synthesized literature regarding the discrepancy between circulating HDL cholesterol concentrations measured in clinical trials and cardiovascular outcomes, and evaluated conditions where impaired HDL function contributes to vascular disease.
What was found
The abstract reports no numerical data. It notes conceptually that foam cell cholesterol efflux mediated by HDL is an antiatherogenic mechanism, but static HDL cholesterol concentration correlates inconsistently with dynamic HDL function and RCT efficacy.
Why it matters
This review explains why therapeutic trials aimed strictly at elevating plasma HDL cholesterol mass failed to reduce cardiovascular events, highlighting the need to target and measure HDL biological function instead.
Limits
As a narrative review, this paper provides expert perspective and mechanistic reasoning rather than systematic review methodology or new empirical human data. No quantitative effect sizes or study sample sizes are reported in the abstract.
Cited by
- contradicts HDL particles can penetrate the inner layer of the arterial wall, bind to LDL, absorb cholesterol and triglycerides, and transport them back to the liver.