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Updated: Aug 31, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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トラフ2のタンパク質分解はドクソルビシン心筋病におけるミトコンドリア機能障害を媒介する

Rimpy Dhingra1, Inna Rabinovich-Nikitin1, Sonny Rothman1

  • 1Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology (R.D., I.R.-N., S.R., M.G., H.G., V.M., D.S.J., K.N.A., S.D., L.A.K.), Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, Canada.

Circulation
|August 19, 2022
PubMed
まとめ

ドクソルビシン (DOX) 治療は,心臓の生存信号に不可欠なタンパク質であるTRAF2を減少させます. この障害は,TNFα媒介による死に対する心臓細胞の感受性を高めることで,DOX誘発の心臓毒性につながる.

キーワード:
TNF受容体関連因子2ドクソルビシンアポトーシスタンパク質の阻害剤ミトコンドリア筋細胞,心臓プロテアソームエンドペプチダゼ複合体腫瘍死滅因子アルファ

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