Evidence map›Paper›PMID 18423408›Full record

ReviewProgress in lipid research2008

Cholesterol homeostasis and the escape tendency (activity) of plasma membrane cholesterol.

Yvonne Lange, Theodore L Steck

Open access · greenAbstract readReview
In one paragraph

Review in Progress in lipid research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
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

70 citing papers in PubMed, 154 citations in OpenAlex.

  1. Article
  2. Article
  3. Critique of a Radically New Model for Plasma Membrane Bilayer Organization.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  4. Article
  5. Article
  6. Synthetic Lipid Biology.Chemical reviews · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Different Pathways of Cellular Cholesterol Efflux.Cell biochemistry and biophysics · 2022
    Review
  16. Article
  17. Specificity of ABCA7-mediated cell lipid efflux.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022
    Article
  18. Article
  19. Article
  20. Review

10 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.

Yvonne LangeDepartment of Pathology, Rush University Medical Center, Chicago, IL 60612, United States. ylange@rush.edu
Theodore L Steck
Rush University Medical Center · USUniversity of Chicago · US

Funding

THE DYNAMICS OF CHOLESTEROL IN MEMBRANESR01HL028448 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI LANGE, YVONNE · 1985 to 2012
$2.9M
DISPOSITION AND MOVEMENT OF CHOLESTEROL IN CELLSR55HL028448 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI LANGE, YVONNE · 1992 to 1992
–
NHLBI NIH HHS HL28448NHLBI NIH HHS R01 HL028448
6 · The paper itself

Abstract

We review evidence that sterols can form stoichiometric complexes with certain bilayer phospholipids, and sphingomyelin in particular. These complexes appear to be the basis for the formation of condensed and ordered liquid phases, (micro)domains and/or rafts in both artificial and biological membranes. The sterol content of a membrane can exceed the complexing capacity of its phospholipids. The excess, uncomplexed membrane sterol molecules have a relatively high escape tendency, also referred to as fugacity or chemical activity (and, here, simply activity). Cholesterol is also activated when certain membrane intercalating amphipaths displace it from the phospholipid complexes. Active cholesterol projects from the bilayer and is therefore highly susceptible to attack by cholesterol oxidase. Similarly, active cholesterol rapidly exits the plasma membrane to extracellular acceptors such as cyclodextrin and high-density lipoproteins. For the same reason, the pool of cholesterol in the ER (endoplasmic reticulum) increases sharply when cell surface cholesterol is incremented above the physiological set-point; i.e., equivalence with the complexing phospholipids. As a result, the escape tendency of the excess cholesterol not only returns the plasma membrane bilayer to its set-point but also serves as a feedback signal to intracellular homeostatic elements to down-regulate cholesterol accretion.

Indexed as

Cell MembraneCholesterolCholesterol OxidaseHomeostasisHumansLipid BilayersPhase TransitionPhospholipidsSterolsCholesterolCholesterol OxidaseLipid BilayersPhospholipidsSterols

Identifiers

PMID18423408
PMCPMC2659507
OpenAlexW2092735428

What OpenQuestion holds

Textmetadata
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.