Drp1-依存型ミトコンドリア・オートファギーは,圧力過負荷によるミトコンドリア機能障害と心不全に対する保護的役割を果たす.

Akihiro Shirakabe ¹, Peiyong Zhai ¹, Yoshiyuki Ikeda ¹

¹From Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., P.Z., Y.I., T.S., Y.M., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medicine and Bioregulatory Science, Kyushu University, Fukuoka, Japan (M.N.); Division of Cardiovascular Surgery, Department of Surgery, Veterans General Hospital, National Yang-Ming University School of Medicine, Taiwan (C.-P.H.); Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan (K.E.); Department of Cardiovascular Research, Development, and Translational Medicine, Graduate School of Medical Science, Kyushu University Hospital, Fukuoka, Japan (K.E.); and Center for Autophagy Research, Department of Internal Medicine, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas (B.L.).
²From Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., P.Z., Y.I., T.S., Y.M., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medicine and Bioregulatory Science, Kyushu University, Fukuoka, Japan (M.N.); Division of Cardiovascular Surgery, Department of Surgery, Veterans General Hospital, National Yang-Ming University School of Medicine, Taiwan (C.-P.H.); Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan (K.E.); Department of Cardiovascular Research, Development, and Translational Medicine, Graduate School of Medical Science, Kyushu University Hospital, Fukuoka, Japan (K.E.); and Center for Autophagy Research, Department of Internal Medicine, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas (B.L.). sadoshju@njms.rutgers.edu.

⁰From Department of Cell Biology and Molecular Medicine, Rutgers-New Jersey Medical School, Newark (A.S., P.Z., Y.I., T.S., Y.M., J.S.); Department of Cardiovascular Medicine and Hypertension, Graduate School of Medical and Dental Science, Kagoshima University, Japan (Y.I.); Department of Medicine and Bioregulatory Science, Kyushu University, Fukuoka, Japan (M.N.); Division of Cardiovascular Surgery, Department of Surgery, Veterans General Hospital, National Yang-Ming University School of Medicine, Taiwan (C.-P.H.); Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan (K.E.); Department of Cardiovascular Research, Development, and Translational Medicine, Graduate School of Medical Science, Kyushu University Hospital, Fukuoka, Japan (K.E.); and Center for Autophagy Research, Department of Internal Medicine, and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas (B.L.).

まとめ

ミトコンドリアのオートファギーは一時的に活性化され,心不全では抑制されます. ダウンレギュレーションは心臓の機能不全を誘発しますがミトコンドリアのオートファギーの回復は圧力過負荷での結果を改善します

Drp1-依存型ミトコンドリア・オートファギーは,圧力過負荷によるミトコンドリア機能障害と心不全に対する保護的役割を果たす.

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Drp1-依存型ミトコンドリア・オートファギーは,圧力過負荷によるミトコンドリア機能障害と心不全に対する保護的役割を果たす.

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