Evidence map›Paper›PMID 22720042›Full record

ArticlePloS one2012

Vanin-1 pantetheinase drives smooth muscle cell activation in post-arterial injury neointimal hyperplasia.

K Jagadeesha Dammanahalli, Stephanie Stevens, Robert Terkeltaub

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Synthesis of Potent Vanin-1 Inhibitors Labelled With Carbon-14 and Deuterium.Journal of labelled compounds & radiopharmaceuticals · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Vanin 1: Its Physiological Function and Role in Diseases.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Role of the Vanins-Myeloperoxidase Axis in Colorectal Carcinogenesis.International journal of molecular sciences · 2017
    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.

K Jagadeesha DammanahalliSan Diego VA Healthcare System and Department of Medicine, University of California San Diego, San Diego, California, United States of America.
Stephanie Stevens
Robert Terkeltaub
VA San Diego Healthcare System · US

Funding

NPP1 and Molecular Mechanisms in Artery CalcificationR01HL077360 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI TERKELTAUB, ROBERT A. · 2004 to 2012
$2.2M
Transglutaminase 2 in Arterial Calcification and AtherosclerosisR01HL087252 · NHLBI · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI TERKELTAUB, ROBERT A. · 2008 to 2011
$1.4M
NHLBI NIH HHS HL077360NHLBI NIH HHS HL087252NHLBI NIH HHS R01 HL077360NHLBI NIH HHS R01 HL087252
6 · The paper itself

Abstract

The pantetheinase vanin-1 generates cysteamine, which inhibits reduced glutathione (GSH) synthesis. Vanin-1 promotes inflammation and tissue injury partly by inducing oxidative stress, and partly by peroxisome proliferator-activated receptor gamma (PPARγ) expression. Vascular smooth muscle cells (SMCs) contribute to neointimal hyperplasia in response to injury, by multiple mechanisms including modulation of oxidative stress and PPARγ. Therefore, we tested the hypothesis that vanin-1 drives SMC activation and neointimal hyperplasia. We studied reactive oxygen species (ROS) generation and functional responses to platelet-derived growth factor (PDGF) and the pro-oxidant diamide in cultured mouse aortic SMCs, and also assessed neointima formation after carotid artery ligation in vanin-1 deficiency. Vnn1(-/-) SMCs demonstrated decreased oxidative stress, proliferation, migration, and matrix metalloproteinase 9 (MMP-9) activity in response to PDGF and/or diamide, with the effects on proliferation linked, in these studies, to both increased GSH levels and PPARγ expression. Vnn1(-/-) mice displayed markedly decreased neointima formation in response to carotid artery ligation, including decreased intima:media ratio and cross-sectional area of the neointima. We conclude that vanin-1, via dual modulation of GSH and PPARγ, critically regulates the activation of cultured SMCs and development of neointimal hyperplasia in response to carotid artery ligation. Vanin-1 is a novel potential therapeutic target for neointimal hyperplasia following revascularization.

Indexed as

AmidohydrolasesAnimalsArteriesBase SequenceBlotting, WesternDNA PrimersElectrophoresis, Polyacrylamide GelGPI-Linked ProteinsHyperplasiaMiceMice, KnockoutMuscle, SmoothOxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionAmidohydrolasesDNA PrimersGPI-Linked ProteinspantetheinaseReactive Oxygen Species

Identifiers

PMID22720042
PMCPMC3374784
OpenAlexW2088519994

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.