ArticleJCI insight2020
Disturbed flow-induced Gs-mediated signaling protects against endothelial inflammation and atherosclerosis.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Article
- Mechanobiology of cancer-associated thrombosis: from molecular mechanisms to therapeutic innovation.Journal of nanobiotechnology · 2026Review
- Article
- Genome-Wide Pleiotropy Analysis Identifies Shared and Opposing Pathways Influencing Coronary Artery Disease and Cancer.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Endothelial Gsα deficiency promotes ferroptosis and exacerbates atherosclerosis in apolipoprotein E-deficient mice via the inhibition of NRF2 signaling.Acta pharmacologica Sinica · 2025Article
- Endothelial cells under disturbed flow release extracellular vesicles to promote inflammatory polarization of macrophages and accelerate atherosclerosis.BMC biology · 2025Article
- Coronary Artery Disease Risk Variant Dampens the Expression of CALCRL by Reducing HSF Binding to Shear Stress Responsive Enhancer in Endothelial Cells In Vitro.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Gsα Regulates Macrophage Foam Cell Formation During Atherosclerosis.Circulation research · 2024Article
- Nuclear mechanosensing of the aortic endothelium in health and disease.Disease models & mechanisms · 2023Review
- CircRNA/lncRNA-miRNA-mRNA network and gene landscape in calcific aortic valve disease.BMC genomics · 2023Article
- Constructing Lipoparticles Capable of Endothelial Cell-Derived Exosome-Mediated Delivery of Anti-miR-33a-5p to Cultured Macrophages.Current issues in molecular biology · 2023Article
- A multi-target protective effect of Danggui-Shaoyao-San on the vascular endothelium of atherosclerotic mice.BMC complementary medicine and therapies · 2023Article
- Suppression of CCL2 angiocrine function by adrenomedullin promotes tumor growth.The Journal of experimental medicine · 2023Article
- More than Just a Monolayer: the Multifaceted Role of Endothelial Cells in the Pathophysiology of Atherosclerosis.Current atherosclerosis reports · 2022Review
- Specialized Proresolving Lipid Mediators: A Potential Therapeutic Target for Atherosclerosis.International journal of molecular sciences · 2022Review
- Intersecting single-cell transcriptomics and genome-wide association studies identifies crucial cell populations and candidate genes for atherosclerosis.European heart journal open · 2022Article
- Endothelial G protein stimulatory α-subunit is a critical regulator of post-ischemic angiogenesis.Frontiers in cardiovascular medicine · 2022Article
- Mechanosensitive Piezo1 Channel Evoked-Mechanical Signals in Atherosclerosis.Journal of inflammation research · 2021Review
- Peripheral Artery Tonometry Reveals Impaired Endothelial Function before Percutaneous Coronary Intervention in Patients with Periprocedural Myocardial Injury.Journal of interventional cardiology · 2021Article
- Vascular Endothelial Senescence: Pathobiological Insights, Emerging Long Noncoding RNA Targets, Challenges and Therapeutic Opportunities.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis develops preferentially in areas of the arterial system, in which blood flow is disturbed. Exposure of endothelial cells to disturbed flow has been shown to induce inflammatory signaling, including NF-κB activation, which leads to the expression of leukocyte adhesion molecules and chemokines. Here, we show that disturbed flow promotes the release of adrenomedullin from endothelial cells, which in turn activates its Gs-coupled receptor calcitonin receptor-like receptor (CALCRL). This induces antiinflammatory signaling through cAMP and PKA, and it results in reduced endothelial inflammation in vitro and in vivo. Suppression of endothelial expression of Gαs, the α subunit of the G-protein Gs; CALCRL; or adrenomedullin leads to increased disturbed flow-induced inflammatory signaling in vitro and in vivo. Furthermore, mice with induced endothelial-specific deficiency of Gαs, CALCRL, or adrenomedullin show increased atherosclerotic lesions. Our data identify an antiinflammatory signaling pathway in endothelial cells stimulated by disturbed flow and suggest activation of the endothelial adrenomedullin/CALCRL/Gs system as a promising approach to inhibit progression of atherosclerosis.
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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.