ArticleEndocrinology2008
Central role of Gq in the hypertrophic signal transduction of angiotensin II in vascular smooth muscle cells.
Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- VSMC-specific TRPC1 deletion attenuates angiotensin II-induced hypertension and cardiovascular remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Article
- ZFP36 Regulates Vascular Smooth Muscle Contraction and Maintains Blood Pressure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular Effects of Auto-Antibodies on Angiotensin II Type 1 Receptor Signaling and Cell Proliferation.International journal of molecular sciences · 2022Article
- Article
- Activation pathway of a G protein-coupled receptor uncovers conformational intermediates as targets for allosteric drug design.Nature communications · 2021Article
- High NaBiomedicines · 2021Review
- The Role of β-Arrestin Proteins in Organization of Signaling and Regulation of the AT1 Angiotensin Receptor.Frontiers in endocrinology · 2019Review
- BRET-based assay to monitor EGFR transactivation by the ATBiochemical pharmacology · 2018Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Natriuretic peptide receptor-C-mediated attenuation of vascular smooth muscle cell hypertrophy involves Gqα/PLCβ1 proteins and ROS-associated signaling.Pharmacology research & perspectives · 2018Article
- AT1 receptor signaling pathways in the cardiovascular system.Pharmacological research · 2017Review
- Vascular ADAM17 as a Novel Therapeutic Target in Mediating Cardiovascular Hypertrophy and Perivascular Fibrosis Induced by Angiotensin II.Hypertension (Dallas, Tex. : 1979) · 2016Article
- Epidermal Growth Factor Receptor Transactivation: Mechanisms, Pathophysiology, and Potential Therapies in the Cardiovascular System.Annual review of pharmacology and toxicology · 2016Article
- Role of epidermal growth factor receptor and endoplasmic reticulum stress in vascular remodeling induced by angiotensin II.Hypertension (Dallas, Tex. : 1979) · 2015Article
- A functional siRNA screen identifies genes modulating angiotensin II-mediated EGFR transactivation.Journal of cell science · 2013Article
- ADAM17 silencing by adenovirus encoding miRNA-embedded siRNA revealed essential signal transduction by angiotensin II in vascular smooth muscle cells.Journal of molecular and cellular cardiology · 2013Article
- Functional relevance of biased signaling at the angiotensin II type 1 receptor.Endocrine, metabolic & immune disorders drug targets · 2011Review
- Caveolin-1 negatively regulates a metalloprotease-dependent epidermal growth factor receptor transactivation by angiotensin II.Journal of molecular and cellular cardiology · 2011Article
- The Rho exchange factor Arhgef1 mediates the effects of angiotensin II on vascular tone and blood pressure.Nature medicine · 2010Article
- Bile acid reflux contributes to development of esophageal adenocarcinoma via activation of phosphatidylinositol-specific phospholipase Cgamma2 and NADPH oxidase NOX5-S.Cancer research · 2010Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The angiotensin II (AngII) type 1 receptor (AT(1)) plays a critical role in hypertrophy of vascular smooth muscle cells (VSMCs). Although it is well known that G(q) is the major G protein activated by the AT(1) receptor, the requirement of G(q) for AngII-induced VSMC hypertrophy remains unclear. By using cultured VSMCs, this study examined the requirement of G(q) for the epidermal growth factor receptor (EGFR) pathway, the Rho-kinase (ROCK) pathway, and subsequent hypertrophy. AngII-induced intracellular Ca(2+) elevation was completely inhibited by a pharmacological G(q) inhibitor as well as by adenovirus encoding a G(q) inhibitory minigene. AngII (100nm)-induced EGFR transactivation was almost completely inhibited by these inhibitors, whereas these inhibitors only partially inhibited AngII (100nm)-induced phosphorylation of a ROCK substrate, myosin phosphatase target subunit-1. Stimulation of VSMCs with AngII resulted in an increase of cellular protein and cell volume but not in cell number. The G(q) inhibitors completely blocked these hypertrophic responses, whereas a G protein-independent AT(1) agonist did not stimulate these hypertrophic responses. In conclusion, G(q) appears to play a major role in the EGFR pathway, leading to vascular hypertrophy induced by AngII. Vascular G(q) seems to be a critical target of intervention against cardiovascular diseases associated with the enhanced renin-angiotensin system.
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Registered trials
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.