Evidence map›Paper›PMID 18855617›Full record

ReviewCurrent drug targets2008

Enhancing cardiovascular dynamics by inhibition of thrombospondin-1/CD47 signaling.

Jeff S Isenberg, William A Frazier, Murali C Krishna, David A Wink, David D Roberts

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Review
  4. Anti-CD47 antibody treatment attenuates liver inflammation and fibrosis in experimental non-alcoholic steatohepatitis models.Liver international : official journal of the International Association for the Study of the Liver · 2022
    Article
  5. Article
  6. Thrombospondins: A Role in Cardiovascular Disease.International journal of molecular sciences · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. The matricellular protein thrombospondin-1 globally regulates cardiovascular function and responses to stress via CD47.Matrix biology : journal of the International Society for Matrix Biology · 2012
    Review
  14. Article
  15. Age-dependent regulation of skeletal muscle mitochondria by the thrombospondin-1 receptor CD47.Matrix biology : journal of the International Society for Matrix Biology · 2011
    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

5 authors at 1 institution in 1 country.

Jeff S IsenbergLaboratory of Pathology and Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
William A Frazier
Murali C Krishna
David A Wink
David D Roberts
National Institutes of Health · US

Funding

Cellular Interactions with ThrombospondinZIASC009172 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$17.9M
Integrin Associated Protein in a Thrombospondin ReceptorR01HL054390 · NHLBI · WASHINGTON UNIVERSITY · PI FRAZIER, WILLIAM A · 2002 to 2012
$3.4M
INTEGRIN ASSOCIATED PROTEIN (IAP) IG DOMAIN FUNCTIONR01GM057573 · NIGMS · WASHINGTON UNIVERSITY · PI FRAZIER, WILLIAM A · 1998 to 2006
$1.9M
CELLULAR INTERACTIONS WITH THROMBOSPONDINZ01SC009172 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 1996 to 2008
$1.7M
Roles of Glycoconjugates and Redox Signaling in Tumor BiologyZ01SC009174 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 1996 to 2008
$453k
Integrin Associated Protein in a Thrombospondin ReceptorR56HL054390 · NHLBI · WASHINGTON UNIVERSITY · PI FRAZIER, WILLIAM A · 2007 to 2007
$380k
Intramural NIH HHS Z01 SC009172Intramural NIH HHS Z01 SC009174NHLBI NIH HHS HL54390NHLBI NIH HHS R01 HL054390NHLBI NIH HHS R56 HL054390NIGMS NIH HHS GM57573NIGMS NIH HHS R01 GM057573
6 · The paper itself

Abstract

Activation of soluble guanylate cyclase by nitric oxide (NO) controls signaling pathways that play critical roles in normal vascular physiology and in the pathogenesis of cardiovascular disease. We have identified the secreted protein thrombospondin-1 as a key regulator of NO signaling. Thrombospondin-1 limits the angiogenic activity of NO in endothelial cells, its vasodilator activity in vascular smooth muscle, and its antithrombotic activity in platelets. Loss of either thrombospondin-1 or its receptor CD47 in transgenic mice results in hyperdynamic responses to NO and reveals the importance of this pathway in normal physiology. Thrombospondin-1 and CD47 null mice show improved abilities to respond to ischemic stress, suggesting that therapeutic targeting of this pathway could benefit patients with a variety of ischemic conditions. We review the preclinical development of therapeutics targeting thrombospondin-1 or CD47 for improving survival of fixed ischemia, ischemia due to aging and peripheral vascular disease, and skin grafting.

Indexed as

AnimalsCardiovascular DiseasesCD47 AntigenHumansMuscle, Smooth, VascularNitric OxideSignal TransductionThrombospondin 1CD47 AntigenNitric OxideThrombospondin 1

Identifiers

PMID18855617
PMCPMC2575641
OpenAlexW2110416513

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.