The DOI matches its Crossref record; 468 of the 468 references it cites were found in a registry or an index.
eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues
Abstract
Nitric oxide production in response to flow-dependent shear forces applied on the surface of endothelial cells is a fundamental mechanism of regulation of vascular tone, peripheral resistance, and tissue perfusion. This implicates the concerted action of multiple upstream "mechanosensing" molecules reversibly assembled in signalosomes recruiting endothelial nitric oxide synthase (eNOS) in specific subcellular locales, e.g., plasmalemmal caveolae. Subsequent short- and long-term increases in activity and expression of eNOS translate this mechanical stimulus into enhanced NO production and bioactivity through a complex transcriptional and posttranslational regulation of the enzyme, including by shear-stress responsive transcription factors, oxidant stress-dependent regulation of transcript stability, eNOS regulatory phosphorylations, and protein-protein interactions. Notably, eNOS expressed in cardiac myocytes is amenable to a similar regulation in response to stretching of cardiac muscle cells and in part mediates the length-dependent increase in cardiac contraction force. In addition to short-term regulation of contractile tone, eNOS mediates key aspects of cardiac and vascular remodeling, e.g., by orchestrating the mobilization, recruitment, migration, and differentiation of cardiac and vascular progenitor cells, in part by regulating the stabilization and transcriptional activity of hypoxia inducible factor in normoxia and hypoxia. The continuum of the influence of eNOS in…
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“Regulation of eNOS is also intimately related to the physical forces important in vascular function such as shear stress induced by blood flow (27, 31).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [31]
In the citing paper
“At the extreme of this spectrum, it is known that for inducible NOS to kill microbes, parasites, or cancer cells, high levels of NO are needed to destroy FeS centers and respiratory proteins in the target organism (28, 31, 32, 46).”
From What Part of NO Don't You Understand? Some Answers to the Cardinal Questions in Nitric Oxide Biology (2010) · cites this paper as [31]
In the citing paper
“It produces relatively low quantities of NO, and its activity is controlled by Ca2+ and calmodulin, post-translational modifications [72, 73], and physical forces such as shear stress [74, 75].”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [74]
Citations
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Nitric oxide signalling in cardiovascular health and disease
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Metadata
- Authors
- Balligand, J.-L., Feron, O., & Dessy, C.
- Affiliations
- UCLouvain (BE)
- Venue
- Physiological Reviews
- Publisher
- American Physiological Society
- Published
- 2009-04
- Volume
- 89
- Issue
- 2
- Pages
- 481-534
- ISSN
- 0031-9333 (ISSN-L)
- 1522-1210
- OpenAlex
- W2142274635
- Cited by
- 477
- References
- 466
- Citations by year
- 2026: 18 · 2025: 15 · 2024: 14 · 2023: 19 · 2022: 27 · 2021: 22 · 2020: 20 · 2019: 18 · 2018: 30 · 2017: 33 · 2016: 30 · 2015: 34 · 2014: 37 · 2013: 37 · 2012: 38
- FWCI
- 4.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Physiological Reviews (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Keywords
- endothelial nitric oxide synthase, mechanotransduction, shear stress, nitric oxide production, endothelial cells, caveolae, signalosome, eNOS phosphorylation, cardiomyocytes, cardiac remodeling, vascular remodeling, progenitor cell mobilization, hypoxia-inducible factor, blood pressure regulation, hemodynamic overload
- MeSH terms
- Animals, Cardiovascular Physiological Phenomena, Endothelium, Vascular, Humans, Myocardial Contraction, Myocardium, Vasoconstriction, Mechanotransduction, Cellular, Nitric Oxide Synthase Type III
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