Evidence map›Paper›PMID 21626289›Full record

ReviewCell and tissue research2012

Transforming growth factor-β and atherosclerosis: interwoven atherogenic and atheroprotective aspects.

Ian Toma, Timothy A McCaffrey

Open access · greenAbstract readReview
In one paragraph

Review in Cell and tissue research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 5% 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

120 citing papers in PubMed, 2 syntheses or guidelines pooled it, 201 citations in OpenAlex.

  1. Pooled it
  2. Association Between Transforming Growth Factor-β1 Polymorphisms and Ischemic Stroke Susceptibility: A Meta-Analysis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. USP5 Stabilizes TGFBR1 to Drive Vascular Smooth Muscle Cell Senescence and Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Review
  9. TGF-β and TNF-α Signaling Crosstalk in Human Coronary Artery Cells.International journal of molecular sciences · 2026
    Article
  10. Article
  11. Article
  12. Cardioprotective Role of CalhexCell biochemistry and biophysics · 2026
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. ThebioRxiv : the preprint server for biology · 2025
    Article
  20. Article

60 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 1 institution in 1 country.

Ian TomaDepartment of Medicine, Division of Genomic Medicine, The George Washington University Medical Center, 2300 I Street NW. Ross Hall 443, Washington, DC 20037, USA.
Timothy A McCaffrey
Washington University Medical Center · US

Funding

TGF-BETA 1 RECEPTORS IN RESTENOSIS AND AGINGR37AG012712 · NIA · GEORGE WASHINGTON UNIVERSITY · PI MCCAFFREY, TIMOTHY A. · 2001 to 2009
$2.9M
NIA NIH HHS R37 AG012712
6 · The paper itself

Abstract

Age-related progression of cardiovascular disease is by far the largest health problem in the US and involves vascular damage, progressive vascular fibrosis and the accumulation of lipid-rich atherosclerotic lesions. Advanced lesions can restrict flow to key organs and can trigger occlusive thrombosis resulting in a stroke or myocardial infarction. Transforming growth factor-beta (TGF-β) is a major orchestrator of the fibroproliferative response to tissue damage. In the early stages of repair, TGF-β is released from platelets and activated from matrix reservoirs; it then stimulates the chemotaxis of repair cells, modulates immunity and inflammation and induces matrix production. At later stages, it negatively regulates fibrosis through its strong antiproliferative and apoptotic effects on fibrotic cells. In advanced lesions, TGF-β might be important in arterial calcification, commonly referred to as "hardening of the arteries". Because TGF-β can signal through multiple pathways, namely the SMADs, a MAPK pathway and the Rho/ROCK pathways, selective defects in TGF-β signaling can disrupt otherwise coordinated pathways of tissue regeneration. TGF-β is known to control cell proliferation, cell migration, matrix synthesis, wound contraction, calcification and the immune response, all being major components of the atherosclerotic process. However, many of the effects of TGF-β are essential to normal tissue repair and thus, TGF-β is often thought to be "atheroprotective". The present review attempts to parse systematically the known effects of TGF-β on both the major risk factors for atherosclerosis and to isolate the role of TGF-β in the many component pathways involved in atherogenesis.

Indexed as

AnimalsAtherosclerosisFibrosisHumansInflammationReceptors, Transforming Growth Factor betaRisk FactorsSmad ProteinsTransforming Growth Factor betaWound HealingReceptors, Transforming Growth Factor betaSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID21626289
PMCPMC4915479
OpenAlexW1975451889

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.