ReviewJournal of vascular surgery2008
Induction of vascular atrophy as a novel approach to treating restenosis. A review.
Review in Journal of vascular surgery, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Thrombospondin-4 regulates apoptosis of vascular smooth muscle cells after artery transplanted into vein.Scientific reports · 2025Article
- Identification and Analysis of Differentially Expressed Genes in Human Saphenous Vein Endothelial Cells Overexpressing Domain-Containing mTOR-Interacting Protein (DEPTOR) by RNA-Seq.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Intravascular ultrasound assessment of the effect of laser energy on the arterial wall during the treatment of femoro-popliteal lesions: a CliRpath excimer laser system to enlarge lumen openings (CELLO) registry study.The international journal of cardiovascular imaging · 2018Article
- Distinctive effects of CD34- and CD133-specific antibody-coated stents on re-endothelialization and in-stent restenosis at the early phase of vascular injury.Regenerative biomaterials · 2015Article
- Effect of imatinib mesylate and rapamycin on the preformed intimal hyperplasia in rat carotid injury model.Annals of surgical treatment and research · 2015Article
- Intimal hyperplasia in loop-injured carotid arteries is attenuated in transglutaminase 2-null mice.Journal of Korean medical science · 2014Article
- Different Responses of Neointimal Cells to Imatinib Mesylate and Rapamycin Compared with Normal Vascular Smooth Muscle Cells.Vascular specialist international · 2014Article
- Inhibition of intimal hyperplasia by local perivascular application of rapamycin and imatinib mesilate after carotid balloon injury.Journal of the Korean Surgical Society · 2013Article
- The role of atherectomy in the treatment of lower extremity peripheral artery disease.BMC surgery · 2012Review
- A link between smooth muscle cell death and extracellular matrix degradation during vascular atrophy.Journal of vascular surgery · 2011Article
- Concomitant proliferation and caspase-3 mediated apoptosis in response to low shear stress and balloon injury.The Journal of surgical research · 2010Article
- Cell death-associated ADAMTS4 and versican degradation in vascular tissue.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2009Article
- Caldesmon as a therapeutic target for proliferative vascular diseases.Mini reviews in medicinal chemistry · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Regardless of the type of arterial reconstruction, luminal narrowing (stenosis or restenosis) develops in approximately one third of the vessels. In the past, the focus of research has been on the mechanisms of stenosis (intimal hyperplasia, pathologic remodeling) and pharmacologic approaches to prevention. An alternative approach is to induce intimal atrophy after luminal narrowing has developed, thus limiting treatment to only those patients that develop a problem. This approach to treat established disease by reducing wall mass through induction of cell death and extracellular matrix removal would be particularly useful for treating stenosis in synthetic bypass grafts or stented vessels, in which intimal hyperplasia is the primary mechanism of stenosis. This approach may be applicable as well to other vascular proliferative disorders, such as pulmonary hypertension and chronic transplant arteriopathy. Proof of principle has been shown in experiments with antibodies to platelet-derived growth factor (PDGF) receptors that cause neointimal regression in baboon polytetrafluoroethylene (PTFE) grafts and with angiotensin-converting enzyme inhibitors that induce medial atrophy in hypertensive arteries. Possible molecular targets could include PDGF receptors, A20, and BMP4. Further studies are needed to determine the utility of such a therapeutic approach to vascular disease.
Indexed as
Identifiers
What OpenQuestion holds
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.