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Cited by 680

The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.

Role of TNF-α in vascular dysfunction

Open access
Zhang, Hanrui, Park, Yoonjung, Wu, Junxi, Chen, Xiu ping, Lee, Sewon, Yang, Jiyeon, Dellsperger, Kevin C., Zhang, Cuihua·2009·Clinical Science
DOI 10.1042/cs20080196
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Abstract

Healthy vascular function is primarily regulated by several factors including EDRF (endothelium-dependent relaxing factor), EDCF (endothelium-dependent contracting factor) and EDHF (endothelium-dependent hyperpolarizing factor). Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. However, the exact mechanisms underlying the impaired vascular activity remain unresolved and there is no current scientific consensus. Accumulating evidence suggests that the inflammatory cytokine TNF (tumour necrosis factor)-α plays a pivotal role in the disruption of macrovascular and microvascular circulation both in vivo and in vitro. AGEs (advanced glycation end-products)/RAGE (receptor for AGEs), LOX-1 [lectin-like oxidized low-density lipoprotein receptor-1) and NF-κB (nuclear factor κB) signalling play key roles in TNF-α expression through an increase in circulating and/or local vascular TNF-α production. The increase in TNF-α expression induces the production of ROS (reactive oxygen species), resulting in endothelial dysfunction in many pathophysiological conditions. Lipid metabolism, dietary supplements and physical activity affect TNF-α expression. The interaction between TNF-α and stem cells is also important in terms of vascular repair or regeneration. Careful scrutiny of these factors may help elucidate the mechanisms that induce vascular dysfunction. The focus of the present review is to summarize recent evidence showing the role of TNF-α in vascular dysfunction in cardiovascular disease. We believe these findings may prompt new directions for targeting inflammation in future therapies.

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Metadata

Authors
Zhang, H., Park, Y., Wu, J., Chen, X. P., Lee, S., Yang, J., Dellsperger, K. C., & Zhang, C.
Venue
Clinical Science
Publisher
Portland Press Ltd.
Published
2009-01-08
Volume
116
Issue
3
Pages
219-230
ISSN
  • 0143-5221 (ISSN-L)
  • 1470-8736
DOI
10.1042/cs20080196
OpenAlex
W2012747049
Cited by
680
References
10
FWCI
28.15
Type
journal article
Language
en
Open access
hybrid

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