ReviewVascular biology (Bristol, England)2019
GPCR transactivation signalling in vascular smooth muscle cells: role of NADPH oxidases and reactive oxygen species.
Review in Vascular biology (Bristol, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Phospholipase C-β3 is dispensable for vascular constriction but indispensable for vascular hyperplasia.Experimental & molecular medicine · 2024Article
- Conserved perception of host and non-host signals via the a-pheromone receptor Ste3 inFrontiers in fungal biology · 2024Article
- AFrontiers in cardiovascular medicine · 2024Article
- NOX Dependent ROS Generation and Cell Metabolism.International journal of molecular sciences · 2023Review
- Gαq Is the Specific Mediator of PAR-1 Transactivation of Kinase Receptors in Vascular Smooth Muscle Cells.International journal of molecular sciences · 2022Article
- Brain Protective Effect of Resveratrol via Ameliorating Interleukin-1β-Induced MMP-9-Mediated Disruption of ZO-1 Arranged Integrity.Biomedicines · 2022Article
- Endothelin-1 mediated glycosaminoglycan synthesizing gene expression involves NOX-dependent transactivation of the transforming growth factor-β receptor.Molecular and cellular biochemistry · 2022Article
- Lipopolysaccharide acting via toll-like receptor 4 transactivates the TGF-β receptor in vascular smooth muscle cells.Cellular and molecular life sciences : CMLS · 2022Article
- Vascular smooth muscle cells in intimal hyperplasia, an update.Frontiers in physiology · 2022Review
- The Role of Toll-like Receptors in Atherothrombotic Cardiovascular Disease.ACS pharmacology & translational science · 2020Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The discovery and extension of G-protein-coupled receptor (GPCR) transactivation-dependent signalling has enormously broadened the GPCR signalling paradigm. GPCRs can transactivate protein tyrosine kinase receptors (PTKRs) and serine/threonine kinase receptors (S/TKRs), notably the epidermal growth factor receptor (EGFR) and transforming growth factor-β type 1 receptor (TGFBR1), respectively. Initial comprehensive mechanistic studies suggest that these two transactivation pathways are distinct. Currently, there is a focus on GPCR inhibitors as drug targets, and they have proven to be efficacious in vascular diseases. With the broadening of GPCR transactivation signalling, it is therefore important from a therapeutic perspective to find a common transactivation pathway of EGFR and TGFBR1 that can be targeted to inhibit complex pathologies activated by the combined action of these receptors. Reactive oxygen species (ROS) are highly reactive molecules and they act as second messengers, thus modulating cellular signal transduction pathways. ROS are involved in different mechanisms of GPCR transactivation of EGFR. However, the role of ROS in GPCR transactivation of TGFBR1 has not yet been studied. In this review, we will discuss the involvement of ROS in GPCR transactivation-dependent signalling.
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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.