uPAR欠乏がTGFβ1媒介の線維性改造を誘発し,心周血管状の微環境を形成する

Yulia Goltseva1, Zoya Tsokolaeva2,3, Irina Beloglazova2

  • 1National Medical Research Centre of Cardiology named after academician E.I. Chazov, Moscow, 121552, Russian Federation. YDgoltseva@cardio.ru.

PubMed
まとめ

ウロキナーゼプラズミノゲンアクティベーター受容体 (uPAR) の喪失は,周周微環境を混乱させ,TGFβ1信号伝達を増幅することによって,心筋線維症を悪化させます. これは,PARを線維性心疾患の潜在的な治療標的として強調しています.

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