Nitric oxide and wound repair: Role of cytokines?

Ann Schwentker, Yoram Vodovotz, Richard Weller, Timothy R. Billiar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Wound healing involves platelets, inflammatory cells, fibroblasts, and epithelial cells. All of these cell types are capable of producing nitric oxide (NO), either constitutively or in response to inflammatory cytokines, through the activity of nitric oxide synthases (NOSs): eNOS (NOS3; endothelial NOS) and iNOS (NOS2; inducible NOS), respectively. Indeed, pharmacological inhibition or gene deletion of these enzymes impairs wound healing. The wound healing mechanisms that are triggered by NO appear to be diverse, involving inflammation, angiogenesis, and cell proliferation. All of these processes are controlled by defined cytokine cascades; in many cases, NO appears to modulate these cytokines. In this review, we summarize the history and present state of research on the role of NO in wound healing within the framework of modulation of cytokines.

Original languageEnglish
Pages (from-to)1-10
Number of pages10
JournalNitric Oxide
Volume7
Issue number1
DOIs
Publication statusPublished - 1 Jan 2002

Keywords / Materials (for Non-textual outputs)

  • MCP-1
  • Nitric oxide
  • TGF-β
  • VEGF
  • Wound healing

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