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Cited by 434

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Reversal of impaired wound repair in iNOS-deficient mice by topical adenoviral-mediated iNOS gene transfer.

Open access
Yamasaki, K, Edington, H D, McClosky, C, Tzeng, E, Lizonova, A, Kovesdi, I, Steed, D L, Billiar, T R·1998·Journal of Clinical Investigation

Abstract

Most evidence indicates that nitric oxide plays a role in normal wound repair; however, involvement of inducible nitric oxide synthase (iNOS) has not been established. Experiments were carried out to determine the requirement for iNOS in closing excisional wounds. Wound closure was delayed by 31% in iNOS knockout mice compared with wild-type animals. An identical delay in wound closure was observed in wild-type mice given a continuous infusion of the partially selective iNOS inhibitor N6-(iminoethyl)-L-lysine. Delayed wound healing in iNOS-deficient mice was completely reversed by a single application of an adenoviral vector containing human iNOS cDNA (AdiNOS) at the time of wounding. Reverse transcription PCR identified iNOS mRNA expression in wild-type mice peaking 4-6 d after wounding, and confirmed expression of human iNOS in the adenoviral vector containing human iNOS cDNA-treated animals. These results establish the key role of iNOS in wound closure, and suggest a gene therapy strategy to improve wound healing in iNOS-deficient states such as diabetes, and during steroid treatment.

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Crossref · 10.1172/jci2067

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Cites

  • Nitric oxide, an autocrine regulator of wound fibroblast synthetic function

    Schäffer, M. R., Efron, P. A., Thornton, F. J., Klingel, K., Gross, S. S., & Barbul, A. (1997) · The Journal of Immunology · doi:10.4049/jimmunol.158.5.2375 · Cited by 260 · cited 1×

    “Inhibition of NO synthesis results in a decrease in collagen content in sponges implanted in subcutaneous wounds (14) and a decrease in collagen synthesis by wound fibroblasts in vitro (26), suggesting that NO stimulates collagen synthesis by wound fibroblasts.”
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Metadata

Authors
Yamasaki, K., Edington, H. D., McClosky, C., Tzeng, E., Lizonova, A., Kovesdi, I., Steed, D. L., & Billiar, T. R.
Venue
Journal of Clinical Investigation
Published
1998-03-01
Volume
101
Issue
5
Pages
967-971
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2015776844
Cited by
434
References
1
FWCI
38.77
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Reversal of impaired wound repair in iNOS-deficient mice by topical adenoviral-mediated iNOS gene transfer. https://app.cochat.ai/papers/10.1172/jci2067
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Yamasaki, K., Edington, H. D., McClosky, C., Tzeng, E., Lizonova, A., Kovesdi, I., Steed, D. L., & Billiar, T. R. (1998). Reversal of impaired wound repair in iNOS-deficient mice by topical adenoviral-mediated iNOS gene transfer. Journal of Clinical Investigation. https://doi.org/10.1172/jci2067

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

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