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Cited by 450

The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.

Oxidant stress from nitric oxide synthase–3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load

Open access
Takimoto, Eiki, Champion, Hunter C., Li, Manxiang, Ren, Shuxun, Rodriguez, E. Rene, Tavazzi, Barbara, Lazzarino, Giuseppe, Paolocci, Nazareno, Gabrielson, Kathleen L., Wang, Yibin, Kass, David A.·2005·Journal of Clinical Investigation
DOI 10.1172/jci200521968
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Abstract

Cardiac pressure load stimulates hypertrophy, often leading to chamber dilation and dysfunction. ROS contribute to this process. Here we show that uncoupling of nitric oxide synthase-3 (NOS3) plays a major role in pressure load-induced myocardial ROS and consequent chamber remodeling/hypertrophy. Chronic transverse aortic constriction (TAC; for 3 and 9 weeks) in control mice induced marked cardiac hypertrophy, dilation, and dysfunction. Mice lacking NOS3 displayed modest and concentric hypertrophy to TAC with preserved function. NOS3(-/-) TAC hearts developed less fibrosis, myocyte hypertrophy, and fetal gene re-expression (B-natriuretic peptide and alpha-skeletal actin). ROS, nitrotyrosine, and gelatinase (MMP-2 and MMP-9) zymogen activity markedly increased in control TAC, but not in NOS3(-/-) TAC, hearts. TAC induced NOS3 uncoupling in the heart, reflected by reduced NOS3 dimer and tetrahydrobiopterin (BH4), increased NOS3-dependent generation of ROS, and lowered Ca(2+)-dependent NOS activity. Cotreatment with BH4 prevented NOS3 uncoupling and inhibited ROS, resulting in concentric nondilated hypertrophy. Mice given the antioxidant tetrahydroneopterin as a control did not display changes in TAC response. Thus, pressure overload triggers NOS3 uncoupling as a prominent source of myocardial ROS that contribute to dilatory remodeling and cardiac dysfunction. Reversal of this process by BH4 suggests a potential treatment to ameliorate the pathophysiology of chronic pressure-induced hypertrophy.

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Metadata

Authors
Takimoto, E., Champion, H. C., Li, M., Ren, S., Rodriguez, E. R., Tavazzi, B., Lazzarino, G., Paolocci, N., Gabrielson, K. L., Wang, Y., & Kass, D. A.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2005-04-14
Volume
115
Issue
5
Pages
1221-1231
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci200521968
OpenAlex
W2171466485
Cited by
450
References
65
FWCI
16.60
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Oxidant stress from nitric oxide synthase–3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load. https://app.cochat.ai/papers/10.1172/jci200521968
The paper
Takimoto, E., Champion, H. C., Li, M., Ren, S., Rodriguez, E. R., Tavazzi, B., Lazzarino, G., Paolocci, N., Gabrielson, K. L., Wang, Y., & Kass, D. A. (2005). Oxidant stress from nitric oxide synthase–3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load. Journal of Clinical Investigation. https://doi.org/10.1172/jci200521968

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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.