Format

Send to

Choose Destination
See comment in PubMed Commons below
Expert Opin Ther Targets. 2008 Jun;12(6):677-92. doi: 10.1517/14728222.12.6.677 .

Novel mechanistic concept of platelet inhibition.

Author information

1
University of Massachusetts Medical School, Department of Pathology, 55 Lake Avenue North, Worcester, MA 01655, USA. Alexander.Sigalov@umassmed.edu

Abstract

BACKGROUND:

Activation of circulating platelets by exposed vessel wall collagen is a primary step in the pathogenesis of thrombotic diseases such as heart attack and stroke. Drugs that are capable of blocking platelet activation successfully reduce cardiovascular mortality and morbidity. However, despite intensive research efforts in antithrombotic drug discovery and development, uncontrolled hemorrhage still remains the most common side effect associated with antithrombotic drugs that are currently in use.

OBJECTIVE:

The selective inhibition of glycoprotein VI (GPVI), the central platelet collagen receptor, and/or its signaling may inhibit thrombosis without affecting hemostatic plug formation. However, the mechanism of GPVI signaling is not known, hindering the further development of this promising antithrombotic strategy.

METHODS:

This review focuses on an innovative mechanistic concept of platelet inhibition.

RESULTS/CONCLUSION:

A novel model of GPVI signaling, the signaling chain homooligomerization (SCHOOL) model, has revealed new therapeutic targets for GPVI inhibition, resulting in the development of novel antithrombotic pharmacological approaches and the invention of new platelet inhibitors.

PMID:
18479215
DOI:
10.1517/14728222.12.6.677
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center