Transactivation of EGFR by G protein-coupled receptor in the pathophysiology of intimal hyperplasia

Swastika Sur, Devendra K. Agrawal

    Research output: Contribution to journalArticlepeer-review

    15 Scopus citations

    Abstract

    GPCR-mediated receptor transactivation of EGFR, is one of the effector mechanisms by which GPCR ligands, such as Ang II, thrombin and ET -1, catecholamine, SII-angiotensin, PAF, and uPA that are released at the arterial injury sites, can potentiate intimal hyperplasia. The process of EGFR transactivation can be cognate ligand-dependent or inde-pendent. In cognate ligand-dependent transactivation, ligand-bound GPCR results in the activation of metalloproteases, which sheds membrane tethered growth factor that binds to EGFR on an extracellular ligand-binding domain causing its transactivation. Whereas, in cognate ligand independent transactivation, ligand bound GPCR activates EGFR intracellularly via second messenger system. The mechanism of EGFR transactivation depends on cell type, GPCR ligand and the type of GPCR. In this review article, such cross-talks are critically discussed. The EGFR transactivation generates mitogenic signals leading to various pathological conditions. The goal of this review article is to identify potential targets for therapeutic intervention in clinical conditions related to intimal hyperplasia in cardiovascular system.

    Original languageEnglish
    Pages (from-to)190-201
    Number of pages12
    JournalCurrent Vascular Pharmacology
    Volume12
    Issue number2
    StatePublished - Jan 1 2014

    All Science Journal Classification (ASJC) codes

    • Cardiology and Cardiovascular Medicine
    • Pharmacology
    • Medicine(all)

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