Evidence map›Paper›PMID 29731282›Full record

ReviewJournal of clinical lipidology

Rethinking reverse cholesterol transport and dysfunctional high-density lipoproteins.

Baiba K Gillard, Corina Rosales, Bingqing Xu, Antonio M Gotto, Henry J Pownall

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Cholesterol efflux pathways, inflammation, and atherosclerosis.Critical reviews in biochemistry and molecular biology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Baiba K GillardCenter for Bioenergetics, Houston Methodist Research Institute, Houston, TX, USA; Weill Cornell Medicine, New York, NY, USA.
Corina RosalesCenter for Bioenergetics, Houston Methodist Research Institute, Houston, TX, USA; Weill Cornell Medicine, New York, NY, USA.
Bingqing XuDepartment of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Antonio M GottoCenter for Bioenergetics, Houston Methodist Research Institute, Houston, TX, USA; Weill Cornell Medicine, New York, NY, USA.
Henry J PownallCenter for Bioenergetics, Houston Methodist Research Institute, Houston, TX, USA; Weill Cornell Medicine, New York, NY, USA. Electronic address: hjpownall@HoustonMethodist.org.
BioEnergetics (United States) · USCentral South University · CNWeill Cornell Medicine · US

Funding

Therapeutic Approaches to Dysregulated HDL MetabolismR01HL056865 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI POWNALL, HENRY J. · 1997 to 2015
$5.2M
High Density Lipoprotein Biogenesis and SpeciationR01HL129767 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI POWNALL, HENRY J., ROSALES, CORINA · 2016 to 2019
$2.3M
NHLBI NIH HHS R01 HL056865NHLBI NIH HHS R01 HL129767
6 · The paper itself

Abstract

Human plasma high-density lipoprotein cholesterol concentrations are a negative risk factor for atherosclerosis-linked cardiovascular disease. Pharmacological attempts to reduce atherosclerotic cardiovascular disease by increasing plasma high-density lipoprotein cholesterol have been disappointing so that recent research has shifted from HDL quantity to HDL quality, that is, functional vs dysfunctional HDL. HDL has varying degrees of dysfunction reflected in impaired reverse cholesterol transport (RCT). In the context of atheroprotection, RCT occurs by 2 mechanisms: one is the well-known trans-hepatic pathway comprising macrophage free cholesterol (FC) efflux, which produces early forms of FC-rich nascent HDL (nHDL). Lecithin:cholesterol acyltransferase converts HDL-FC to HDL-cholesteryl ester while converting nHDL from a disc to a mature spherical HDL, which transfers its cholesteryl ester to the hepatic HDL receptor, scavenger receptor B1 for uptake, conversion to bile salts, or transfer to the intestine for excretion. Although widely cited, current evidence suggests that this is a minor pathway and that most HDL-FC and nHDL-FC rapidly transfer directly to the liver independent of lecithin:cholesterol acyltransferase activity. A small fraction of plasma HDL-FC enters the trans-intestinal efflux pathway comprising direct FC transfer to the intestine. SR-B1

Indexed as

AnimalsATP-Binding Cassette TransportersCardiovascular DiseasesCholesterolHumansLipoproteins, HDLPhosphatidylcholine-Sterol O-AcyltransferaseReceptors, LipoproteinScavenger Receptors, Class BATP-Binding Cassette TransportersCholesterolLCAT protein, humanLipoproteins, HDLPhosphatidylcholine-Sterol O-AcyltransferaseReceptors, LipoproteinScavenger Receptors, Class BAtherogenesisATP-binding cassette transporter A1Cholesterol bioavailabilityHDL biogenesisLipoprotein receptorsReverse cholesterol transport

Identifiers

PMID29731282
PMCPMC6064676
OpenAlexW2797942262

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.