Is reverse cholesterol transport a misnomer for suggesting its role in the prevention of atheroma formation?
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanistic commentary with no empirical data
PubMed 7488324 · doi:10.1016/0021-9150(95)05531-z
What was done
This narrative review evaluated the pathways involved in reverse cholesterol transport—including high-density lipoprotein (HDL) uptake of unesterified cell cholesterol, esterification by lecithin-cholesterol-acyl-transferase (LCAT), direct hepatic uptake of HDL-cholesteryl esters, and cholesteryl ester transfer protein (CETP)-mediated transfer to apolipoprotein B-containing lipoproteins—to assess whether the process is uniformly anti-atherogenic.
What was found
The abstract reports no numerical findings or statistical measures. Conceptually, it identifies that while direct HDL-cholesteryl ester uptake by the liver is anti-atherogenic, the indirect CETP-mediated pathway may be atherogenic by raising cholesteryl ester content in VLDL and LDL that can be taken up by arterial wall macrophages. It also notes controversial roles for LCAT and hepatic lipase, alongside anti-atherogenic HDL effects independent of cholesterol removal.
Why it matters
The paper highlights that the term reverse cholesterol transport is overly simplistic because indirect transport pathways can divert cholesterol into atherogenic particles.
Limits
No primary empirical, clinical, or meta-analytic data are reported in the abstract. The discussion is entirely theoretical and mechanism-based.
Cited by
- context In humans, LDL performs the majority of reverse cholesterol transport by receiving cholesterol transferred from HDLs and transporting it back to the liver.