补体 C3 补体因子 D-C3a 受体信号轴调节右心室衰竭的心脏重塑,Nature Communications

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补体 C3 补体因子 D-C3a 受体信号轴调节右心室衰竭的心脏重塑
Nature Communications ( IF 14.7 ) Pub Date : 2022-09-15 , DOI: 10.1038/s41467-022-33152-9
Shogo Ito _{1,

2} , Hisayuki Hashimoto _{1,

3} , Hiroyuki Yamakawa _{1,

3} , Dai Kusumoto _{1,

3} , Yohei Akiba ₁ , Takahiro Nakamura ₁ , Mizuki Momoi ₁ , Jin Komuro ₁ , Toshiomi Katsuki ₁ , Mai Kimura ₁ , Yoshikazu Kishino ₁ , Shin Kashimura ₁ , Akira Kunitomi ₁ , Mark Lachmann ₁ , Masaya Shimojima ₁ , Gakuto Yozu ₁ , Chikaaki Motoda ₁ , Tomohisa Seki _{1,

4} , Tsunehisa Yamamoto ₁ , Yoshiki Shinya ₁ , Takahiro Hiraide ₁ , Masaharu Kataoka _{1,

5} , Takashi Kawakami ₁ , Kunimichi Suzuki ₆ , Kei Ito ₇ , Hirotaka Yada _{7,

8} , Manabu Abe ₉ , Mizuko Osaka ₁₀ , Hiromi Tsuru ₁₀ , Masayuki Yoshida ₁₀ , Kenji Sakimura ₉ , Yoshihiro Fukumoto ₂ , Michisuke Yuzaki ₆ , Keiichi Fukuda ₁ , Shinsuke Yuasa ₁

Affiliation

Department of Cardiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Division of Cardio-Vascular Medicine, Department of Internal Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka, 830-0011, Japan.
Center for Preventive Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Department of Healthcare Information Management, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.
Second Department of Internal Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Department of Physiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Department of Cardiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, 359-8513, Japan.
Department of Cardiology, International University of Health and Welfare, Mita Hospital, 1-4-3 Mita Minatoku, Tokyo, 108-8329, Japan.
Department of Animal Model Development, Brain Research Institute, Niigata University, 1-757 Asahimachi-Dori, Chuo-ku, Niigata, 951-8585, Japan.
Department of Life Sciences and Bioethics, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.

右心室衰竭在任何类型的心力衰竭中都起着至关重要的作用。但其机制尚不清楚，也没有具体的治疗方法。在这里，我们显示右心室主要表达替代补体途径相关基因，包括Cfd和C3aR1。补体 3 ( C3 ) 敲除可减轻右心室衰竭小鼠模型中的右心室功能障碍和纤维化。C3a 由 C3 转化酶复合物从 C3 产生，其中包括必需成分补体因子 D (Cfd)。差价合约敲除小鼠也显示出右心衰竭的减弱。此外，CFD 的血浆浓度与慢性右心衰竭患者的右心衰竭严重程度相关。C3a 受体 (C3aR) 拮抗剂可显着改善小鼠的右心室功能障碍。总之，我们证明了 C3-Cfd-C3aR 轴在右心室衰竭中的关键作用，并强调了右心室衰竭的潜在治疗目标。

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更新日期：2022-09-15

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