Evidence map›Paper›PMID 20932269›Full record

ArticleCardiovascular & hematological disorders drug targets2010

Atherosclerosis-related functions of C-reactive protein.

Alok Agrawal, David J Hammond, Sanjay K Singh

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular & hematological disorders drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Evolution of C-Reactive Protein.Frontiers in immunology · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. CARDIOPROTECTIVE ROLES OF THE CHINESE MEDICINAL FORMULA BAO-XIN-TANG ON ACUTE MYOCARDIAL INFARCTION IN RATS.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2017
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Alok AgrawalDepartment of Pharmacology, East Tennessee State University, Johnson City, TN 37614, USA. agrawal@etsu.edu
David J Hammond
Sanjay K Singh
East Tennessee State University · US

Funding

Structure-Function Relationships of C-Reactive ProteinR01HL071233 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI AGRAWAL, ALOK · 2002 to 2011
$2.6M
NHLBI NIH HHS R01 HL071233NHLBI NIH HHS R01HL071233
6 · The paper itself

Abstract

C-reactive protein (CRP) is secreted by hepatocytes as a pentameric molecule made up of identical monomers, circulates in the plasma as pentamers, and localizes in atherosclerotic lesions. In some cases, localized CRP was detected by using monoclonal antibodies that did not react with native pentameric CRP but were specific for isolated monomeric CRP. It has been reported that, once CRP is bound to certain ligands, the pentameric structure of CRP is altered so that it can dissociate into monomers. Accordingly, the monomeric CRP found in atherosclerotic lesions may be a stationary, ligand-bound, by-product of a ligand-binding function of CRP. CRP binds to modified forms of low-density lipoprotein (LDL). The binding of CRP to oxidized LDL requires acidic pH conditions; the binding at physiological pH is controversial. The binding of CRP to enzymatically-modified LDL occurs at physiological pH; however, the binding is enhanced at acidic pH. Using enzymatically-modified LDL, CRP has been shown to prevent the formation of enzymatically-modified LDL-loaded macrophage foam cells. CRP is neither pro-atherogenic nor atheroprotective in ApoE⁻(/)⁻ and ApoB¹⁰⁰(/)¹⁰⁰Ldlr ⁻(/)⁻ murine models of atherosclerosis, except in one study where CRP was found to be slightly atheroprotective in ApoB¹⁰⁰(/)¹⁰⁰Ldlr ⁻(/)⁻ mice. The reasons for the ineffectiveness of human CRP in murine models of atherosclerosis are not defined. It is possible that an inflammatory environment, such as those characterized by acidic pH, is needed for efficient interaction between CRP and atherogenic LDL during the development of atherosclerosis and to observe the possible atheroprotective function of CRP in animal models.

Indexed as

AnimalsAtherosclerosisC-Reactive ProteinDisease Models, AnimalFoam CellsHumansLipoproteins, LDLMiceC-Reactive ProteinLipoproteins, LDL

Identifiers

PMID20932269
PMCPMC3125067
OpenAlexW2137328580

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.