Evidence map›Paper›PMID 11581304›Full record

ArticleThe Journal of clinical investigation2001

The adhesion receptor CD44 promotes atherosclerosis by mediating inflammatory cell recruitment and vascular cell activation.

C A Cuff, D Kothapalli, I Azonobi, S Chun, Y Zhang, R Belkin, C Yeh, A Secreto, R K Assoian, D J Rader and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

144 citing papers in PubMed, 274 citations in OpenAlex.

  1. Niacin and biosynthesis of PGD₂by platelet COX-1 in mice and humans.The Journal of clinical investigation · 2012 · on this map
    Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Lactylation-related geneFrontiers in immunology · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Research on the Mechanism and Material Basis of Corn (Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  20. Article

84 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

11 authors at 2 institutions in 1 country.

C A CuffThe Wistar Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
D Kothapalli
I Azonobi
S Chun
Y Zhang
R Belkin
C Yeh
A Secreto
R K Assoian
D J Rader
E Puré
The Wistar Institute · USUniversity of Pennsylvania · US

Funding

STUDIES OF PLATELET ADHERENCE TO OSTEOPONTINP01HL062250 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 1999 to 2013
$28.4M
IMMUNOBIOLOGY OF NORMAL AND NEOPLASTIC LYMPHOCYTEST32CA009140 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Malay Haldar, WARREN S PEAR · 1985 to 2026
$16.1M
IMMUNOBIOLOGY OF INTERLUKIN-12R01AI034412 · NIAID · WISTAR INSTITUTE · PI MONTANER, LUIS J. · 1994 to 2003
$1.4M
CELLULAR BASIS OF ANTIATHEROGENESIS BY APOLIPOPROTEIN ER01HL057811 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI RADER, DANIEL JAMES · 1998 to 2001
$686k
NCI NIH HHS CA09140NCI NIH HHS T32 CA009140NHLBI NIH HHS HL57811NHLBI NIH HHS HL62250NHLBI NIH HHS HL66250NHLBI NIH HHS P01 HL062250NIAID NIH HHS AI34412NIAID NIH HHS AI458113NIAID NIH HHS R01 AI034412
6 · The paper itself

Abstract

Atherosclerosis causes most acute coronary syndromes and strokes. The pathogenesis of atherosclerosis includes recruitment of inflammatory cells to the vessel wall and activation of vascular cells. CD44 is an adhesion protein expressed on inflammatory and vascular cells. CD44 supports the adhesion of activated lymphocytes to endothelium and smooth muscle cells. Furthermore, ligation of CD44 induces activation of both inflammatory and vascular cells. To assess the potential contribution of CD44 to atherosclerosis, we bred CD44-null mice to atherosclerosis-prone apoE-deficient mice. We found a 50-70% reduction in aortic lesions in CD44-null mice compared with CD44 heterozygote and wild-type littermates. We demonstrate that CD44 promotes the recruitment of macrophages to atherosclerotic lesions. Furthermore, we show that CD44 is required for phenotypic dedifferentiation of medial smooth muscle cells to the "synthetic" state as measured by expression of VCAM-1. Finally, we demonstrate that hyaluronan, the principal ligand for CD44, is upregulated in atherosclerotic lesions of apoE-deficient mice and that the low-molecular-weight proinflammatory forms of hyaluronan stimulate VCAM-1 expression and proliferation of cultured primary aortic smooth muscle cells, whereas high-molecular-weight forms of hyaluronan inhibit smooth muscle cell proliferation. We conclude that CD44 plays a critical role in the progression of atherosclerosis through multiple mechanisms.

Indexed as

AnimalsAortaApolipoproteins EArteriosclerosisCell AdhesionCell DivisionCells, CulturedFemaleHyaluronan ReceptorsHyaluronic AcidMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularApolipoproteins EHyaluronan ReceptorsHyaluronic AcidVascular Cell Adhesion Molecule-1

Identifiers

PMID11581304
PMCPMC200948
OpenAlexW2109352233

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.