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Cited by 836

The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.

Endothelial Dysfunction, Hemodynamic Forces, and Atherogenesisa

GIMBRONE, MICHAEL A., TOPPER, JAMES N., NAGEL, TOBI, ANDERSON, KEITH R., GARCIA‐CARDEÑA, GUILLERMO·2000·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2000.tb06318.x
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Abstract

A bstract: Phenotypic modulation of endothelium to a dysfunctional state contributes to the pathogenesis of cardiovascular diseases such as atherosclerosis. The localization of atherosclerotic lesions to arterial geometries associated with disturbed flow patterns suggests an important role for local hemodynamic forces in atherogenesis. There is increasing evidence that the vascular endothelium, which is directly exposed to various fluid mechanical forces generated by pulsatile blood flow, can discriminate among these stimuli and transduce them into genetic regulatory events. At the level of individual genes, this regulation is accomplished via the binding of certain transcription factors, such as NFκB and Egr‐1, to shear‐stress response elements (SSREs) that are present in the promoters of biomechanically inducible genes. At the level of multiple genes, distinct patterns of up‐ and downregulation appear to be elicited by exposure to steady laminar shear stresses versus comparable levels of non‐laminar (e.g., turbulent) shear stresses or cytokine stimulation (e.g., IL‐1β). Certain genes upregulated by steady laminar shear stress stimulation (such as eNOS, COX‐2, and Mn‐SOD) support vasoprotective (i.e., anti‐inflammatory, anti‐thrombotic, anti‐oxidant) functions in the endothelium. We hypothesize that the selective and sustained expression of these and related “atheroprotective genes” in the endothelial lining of lesion‐protected areas represents a mechanism whereby hemodynamic forces can influence lesion formation and progression.

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Metadata

Authors
GIMBRONE, M. A., TOPPER, J. N., NAGEL, T., ANDERSON, K. R., & GARCIA‐CARDEÑA, G.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2000-05
Volume
902
Issue
1
Pages
230-240
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2000.tb06318.x
OpenAlex
W2072470670
Cited by
836
References
37
FWCI
15.87
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Endothelial Dysfunction, Hemodynamic Forces, and Atherogenesisa. https://app.cochat.ai/papers/10.1111/j.1749-6632.2000.tb06318.x
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GIMBRONE, M. A., TOPPER, J. N., NAGEL, T., ANDERSON, K. R., & GARCIA‐CARDEÑA, G. (2000). Endothelial Dysfunction, Hemodynamic Forces, and Atherogenesisa. Annals of the New York Academy of Sciences. https://doi.org/10.1111/j.1749-6632.2000.tb06318.x

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.