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Updated: May 10, 2026

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増加したエンドセリン-1レベルは,PKC依存の経路を通じて酸化窒素のホメオスタシスを損なう

Danny Ramzy1, Vivek Rao, Laura C Tumiati

  • 1Heart Transplant Program, University of Toronto, Toronto, Ontario, Canada.

Circulation
|July 6, 2006
PubMed
まとめ

増加したエンドセリン-1 (ET-1) は,タンパク質キナーゼC (PKC) シグナル伝達を通じて,エンドセリアル酸化窒素合成酵素 (eNOS) 発現を阻害することによって,酸化窒素 (NO) 産生を阻害する. ET-1アンタゴニズムは,血管ホメオスタシスを改善する可能性があります.

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