Evidence map›Paper›PMID 23316287›Full record

Trial reportJournal of the American Heart Association2012

Leptin locally synthesized in carotid atherosclerotic plaques could be associated with lesion instability and cerebral emboli.

Jacob Schneiderman, Katrin Schaefer, Frank D Kolodgie, Naphtali Savion, Shlomo Kotev-Emeth, Rima Dardik, Amos J Simon, Moshe Halak, Clara Pariente, Isaac Engelberg and 2 more

Registry-linked trialOpen access · goldAbstract readClinical Trial
In one paragraph

Trial report in Journal of the American Heart Association, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00449306 (Physical,Histological,and Genetic Analyses of Lipid-rich Atherosclerotic Plaques), which is not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 18% 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.

NCT00449306 unknown statusnot on this map

Physical,Histological,and Genetic Analyses of Lipid-rich Atherosclerotic Plaques

TypeobservationalSponsorSheba Medical CenterRan2001 to 2021Enrolled120ConditionsAtherosclerosis, Aortic Aneurysm, Peripheral Vascular Diseases
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Serum Biomarkers in Carotid Artery Disease.Diagnostics (Basel, Switzerland) · 2021
    Review
  8. Review
  9. Observational
  10. Review
  11. Article
  12. Article
  13. Review
  14. Silencing MR-1 attenuates atherosclerosis in ApoEThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  15. Article
  16. Article
  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

12 authors at 4 institutions in 3 countries.

Jacob SchneidermanDepartment of Vascular Surgery and the Gottesdiener Vascular Biology Laboratory, Sheba Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Israel. jschneid72@yahoo.com
Katrin Schaefer
Frank D Kolodgie
Naphtali Savion
Shlomo Kotev-Emeth
Rima Dardik
Amos J Simon
Moshe Halak
Clara Pariente
Isaac Engelberg
Stavros Konstantinides
Renu Virmani
Tel Aviv University · ILSheba Medical Center · ILCVPath Institute · USDemocritus University of Thrace · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnstable carotid plaques cause cerebral emboli. Leptin promotes atherosclerosis and vessel wall remodeling. We hypothesized that carotid atherosclerotic lesion instability is associated with local leptin synthesis. METHODS AND

resultsCarotid endarterectomy plaques from symptomatic (n=40) and asymptomatic patients with progressive stenosis (n=38) were analyzed for local expression of leptin, tumor necrosis factor (TNF)-α, and plasminogen activator inhibitor type 1. All lesions exhibited advanced atherosclerosis inclusive of thick- and thin-cap fibroatheromas or lesion rupture. Symptomatic lesions exhibited more plaque ruptures and macrophage infiltration (P=0.001 and P=0.05, respectively). Symptomatic plaques showed preferential leptin, TNF-α, and plasminogen activator inhibitor type 1 transcript (P=0.03, P=0.04, and P=0.05, respectively). Leptin mRNA and antigen in macrophages and smooth muscle cells were confirmed by in situ hybridization and immunohistochemistry. Plasma leptin levels were not significantly different between groups (P=1.0), whereas TNF-α was significantly increased in symptomatic patients (P=0.006). Human aortic smooth muscle cell culture stimulated by TNF-α, lipopolysaccharide, or lipoteichoic acid revealed 6-, 6.7-, and 6-fold increased secreted leptin antigen, respectively, at 72 hours (P<0.05).

conclusionsNeurologically symptomatic patients overexpress leptin mRNA and synthesize leptin protein in carotid plaque macrophages and smooth muscle cells. Local leptin induction, presumably by TNF-α, could exert paracrine or autocrine effects, thereby contributing to the pathogenesis of lesion instability. CLINICAL

trial registrationURL: www.Clinicaltrials.gov. Unique identifier: NCT00449306.

Indexed as

AdultAgedAged, 80 and overCarotid Artery DiseasesEndarterectomy, CarotidFemaleHumansImmunohistochemistryIn Situ HybridizationIntracranial EmbolismLeptinMaleMiddle AgedMyocytes, Smooth MusclePlaque, AtheroscleroticPlasminogen Activator Inhibitor 1LeptinPlasminogen Activator Inhibitor 1Tumor Necrosis Factor-alphaatherosclerosisleptinmacrophagessmooth muscle cellstumor necrosis factor-α

Identifiers

PMID23316287
PMCPMC3541612
OpenAlexW2127011779

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.