Evidence map›Paper›PMID 23023510›Full record

ReviewCirculation research2012

Novel biological functions of high-density lipoprotein cholesterol.

Chieko Mineo, Philip W Shaul

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 4 pooled it
15.2field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 4 syntheses or guidelines pooled it, 216 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Article
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  10. Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026
    Review
  11. Article
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53 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Chieko MineoDivision of Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Philip W Shaul
Southwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

CHOLESTEROL AND ENDOTHELIAL NO SYNTHASE TRAFFICKINGR01HL058888 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAUL, PHILIP W · 1997 to 2007
$1.9M
NHLBI NIH HHS HL058888NHLBI NIH HHS R01 HL058888
6 · The paper itself

Abstract

In addition to its role in reverse cholesterol transport, high-density lipoprotein (HDL) cholesterol has direct action on numerous cell types that influence cardiovascular and metabolic health. Cellular responses to HDL entail its capacity to invoke cholesterol efflux that causes signal initiation via scavenger receptor class B, type I, and plasma membrane receptor activation by HDL cargo molecules. In endothelial cells and their progenitors, HDL attenuates apoptosis and stimulates proliferation and migration. HDL also has diverse anti-inflammatory actions in both endothelial cells and leukocytes. In vascular smooth muscles, HDL tempers proinflammatory, promigratory, and degradative processes, and through actions on endothelium and platelets HDL is antithrombotic. There are additional actions of HDL of potential cardiovascular consequence that are indirect, including the capacities to promote pancreatic β-cell insulin secretion, to protect pancreatic β cells from apoptosis, and to enhance glucose uptake by skeletal muscle myocytes. Furthermore, HDL decreases white adipose tissue mass, increases energy expenditure, and promotes the production of adipose-derived cytokine adiponectin that has its own vascular-protective properties. Many of these numerous actions of HDL have been observed not only in cell culture and animal models but also in human studies, and assessments of these functions are now being applied to patient populations to better-elucidate which actions of HDL may contribute to its cardioprotective potential and how they can be quantified and targeted. Further work on the many mechanisms of HDL action promises to reveal new prophylactic and therapeutic strategies to optimize both cardiovascular and metabolic health.

Indexed as

AnimalsAtherosclerosisCholesterol, HDLEndothelium, VascularHumansLipoproteins, HDLNitric Oxide SynthaseScavenger Receptors, Class BCholesterol, HDLLipoproteins, HDLNitric Oxide SynthaseSCARB1 protein, humanScavenger Receptors, Class B

Identifiers

PMID23023510
PMCPMC3500606
OpenAlexW2165842273

What OpenQuestion 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 OpenQuestion graph.