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Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology.

Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Research Abstract Details 

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  • Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Abstract Text:

    sadaharu higuchiSadaharu Higuchi,haruhiko ohtsuHaruhiko Ohtsu,hiroyuki suzukiHiroyuki Suzuki,heigoro shiraiHeigoro Shirai,gerald d frankGerald D Frank,satoru eguchiSatoru Eguchi,

    The intracellular signal transduction of AngII (angiotensin II) has been implicated in cardiovascular diseases, such as hypertension, atherosclerosis and restenosis after injury. AT(1) receptor (AngII type-1 receptor), a G-protein-coupled receptor, mediates most of the physiological and pathophysiological actions of AngII, and this receptor is predominantly expressed in cardiovascular cells, such as VSMCs (vascular smooth muscle cells). AngII activates various signalling molecules, including G-protein-derived second messengers, protein kinases and small G-proteins (Ras, Rho, Rac etc), through the AT(1) receptor leading to vascular remodelling. Growth factor receptors, such as EGFR (epidermal growth factor receptor), have been demonstrated to be 'trans'-activated by the AT(1) receptor in VSMCs to mediate growth and migration. Rho and its effector Rho-kinase/ROCK are also implicated in the pathological cellular actions of AngII in VSMCs. Less is known about the endothelial AngII signalling; however, recent studies suggest the endothelial AngII signalling positively, as well as negatively, regulates the NO (nitric oxide) signalling pathway and, thereby, modulates endothelial dysfunction. Moreover, selective AT(1)-receptor-interacting proteins have recently been identified that potentially regulate AngII signal transduction and their pathogenic functions in the target organs. In this review, we focus our discussion on the recent findings and concepts that suggest the existence of the above-mentioned novel signalling mechanisms whereby AngII mediates the formation of cardiovascular diseases.

    Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Publishing Authors By Initials

    s higuchiS Higuchi,h ohtsuH Ohtsu,h suzukiH Suzuki,h shiraiH Shirai,gd frankGD Frank,s eguchiS Eguchi,

    For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

    PUBMED ID PMID:

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    Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Journal Published:

    PUBLICATION TYPE: Review

    Journal: Clinical science (London, England : 1979)

    VOLUME: 112

    Page Numbers: 417-28

    Journal Abbreviation: Clin. Sci.

    ISSN: 1470-8736

    DAY: 3

    MONTH: Apr

    YEAR: 2007

    Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Information

    Number of References: 123

    LANGUAGE: eng

    NlmUniqueID: 7905731

    Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Keywords Mesh Terms:

    KEYWORDS: Signal Transduction

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology. Information

    Substance Name: GTP-Binding Proteins

    Registry Number: EC 3.6.1.-

    Grant and Affiliation Information for Angiotensin II signal transduction through the AT1 receptor: novel insights into mechanisms and pathophysiology.

    AFFILIATION: Cardiovascular Research Center, Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NHLBI

    GRANT: HL076770

    ACRONYM: HL

    MEDLINETA: Clin Sci (Lond)

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