Evidence map›Paper›PMID 19720748›Full record

ArticleMolecular interventions2009

Parstatin, a novel protease-activated receptor 1-derived inhibitor of angiogenesis.

Michael B Duncan, Raghu Kalluri

Abstract read
In one paragraph

Article in Molecular interventions, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

2 authors.

Michael B DuncanDivision of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. mduncan1@bidmc.harvard.edu
Raghu Kalluri

Funding

TYPE IV COLLAGEN IN ALPORT SYNDROME PATHOGENESISR01DK055001 · NIDDK · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KALLURI, RAGHU · 1999 to 2014
$4.3M
Regulation of Angiogenesis by TumstatinR01DK062987 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KALLURI, RAGHU · 2003 to 2006
$1.4M
Role of Fibroblasts in CancerR01CA125550 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KALLURI, RAGHU · 2008 to 2010
$1.1M
Matrix Microenvironment and Liver FibrosisR01AA013913 · NIAAA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KALLURI, RAGHU · 2005 to 2007
$994k
The Biology and Function of BMP-7 in the KidneyR01DK061688 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KALLURI, RAGHU · 2005 to 2007
$746k
NCI NIH HHS CA125550NCI NIH HHS R01 CA125550NIAAA NIH HHS AA13913NIAAA NIH HHS R01 AA013913NIDDK NIH HHS DK55001NIDDK NIH HHS DK 61688NIDDK NIH HHS DK62987NIDDK NIH HHS R01 DK055001NIDDK NIH HHS R01 DK061688NIDDK NIH HHS R01 DK062987
6 · The paper itself

Abstract

Angiogenesis, the process of forming new blood vessels, is a well established and clinically relevant feature of a variety of disease states. Whether blood vessels sprout in a given tissue environment depends on the balance between factors that stimulate angiogenesis and those that impede it. Potent pro-angiogenic factors such as vascular endothelial growth factor (VEGF) have been identified, validated, and successfully used in the clinic. Likewise, anti-angiogenic factors are also emerging as biologically relevant and therapeutically useful entities. PAR1 is a G protein-coupled receptor (GPCR) that participates in hemostasis and vascular development and that mediates the angiogenic activity of thrombin. PAR1 is activated through proteolytic cleavage of its first forty-one extracellular residues by a variety of proteases, most notably thrombin. However, little effort has focused on the forty-one-residue peptide fragment liberated during PAR1 activation. Tsopanoglou and colleagues have now demonstrated that this peptide, parstatin, has intriguing antiangiogenic activity, and, in a follow-up study, they demonstrate its potential pharmacological utility using a rat model of ischemic heart disease.

Indexed as

Drug TherapyAngiogenesis InhibitorsAnimalsGene ExpressionHumansPeptide FragmentsReceptor, PAR-1Angiogenesis InhibitorsPAR-1 receptor (1-41), humanPeptide FragmentsReceptor, PAR-1

Identifiers

PMID19720748
PMCPMC2863086

What OpenQuestion holds

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Registered trials

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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.