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Cited by 274

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Vascular oxidative stress in aging: a homeostatic failure due to dysregulation of NRF2-mediated antioxidant response

Open access
Ungvari, Zoltan, Bailey-Downs, Lora, Sosnowska, Danuta, Gautam, Tripti, Koncz, Peter, Losonczy, Gyorgy, Ballabh, Praveen, de Cabo, Rafael, Sonntag, William E., Csiszar, Anna·2011·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.01134.2010
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Abstract

There is strong evidence showing that aging is associated with vascular oxidative stress, which has been causally linked to the development of cardiovascular diseases. NF-E2-related factor-2 (Nrf2) is a transcription factor, which is activated by reactive oxygen species in the vasculature of young animals leading to the upregulation of various antioxidant genes. The present study was designed to elucidate age-related changes in the homeostatic role of Nrf2-driven free radical detoxification mechanisms in the vasculature. We found that in the aorta of Fischer 344 × Brown Norway rats, aging results in a progressive increase in O 2·−production, and downregulates protein and mRNA expression of Nrf2, which is associated with a decreased nuclear Nrf2 activity and a decrease in the Nrf2 target genes NAD(P)H:quinone oxidoreductase 1, γ-glutamylcysteine synthetase, and heme oxygenase-1. There was an inverse relationship between vascular expression of Nrf2 target genes and age-related increases in the expression of the NF-κB target genes ICAM-1 and IL-6, which was significant by regression analysis. In cultured aorta segments of young (3 mo old) rats treatment with H 2 O 2 and high glucose significantly increases nuclear translocation of Nrf2 and upregulates the expression of Nrf2 target genes. In contrast, in cultured aorta segments of aged (24 mo old) rats, the induction of Nrf2-dependent responses by H 2 O 2 and high glucose are blunted. High glucose-induced vascular oxidative stress was more severe in aortas of aged rats, as shown by the significantly increased H 2 O 2 production in these vessels, compared with responses obtained in aortas from young rats. Moreover, we found that aging progressively increases vascular sensitivity to the proapoptotic effects of H 2 O 2 and high glucose treatments. Taken together, aging is associated with Nrf2 dysfunction in the vasculature, which likely exacerbates age-related cellular oxidative stress and increases sensitivity of aged vessels to oxidative stress-induced cellular damage.

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Metadata

Authors
Ungvari, Z., Bailey-Downs, L., Sosnowska, D., Gautam, T., Koncz, P., Losonczy, G., Ballabh, P., de Cabo, R., Sonntag, W. E., & Csiszar, A.
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2011-08
Volume
301
Issue
2
Pages
H363-H372
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.01134.2010
OpenAlex
W2170389508
Cited by
274
References
4
FWCI
6.58
Type
journal article
Language
en
Open access
green

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