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肾缺血再灌注损伤与内质网应激 被引量:6

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作者 龚慧 万福生
出处 《南昌大学学报(医学版)》 CAS 2010年第1期121-123,共3页 Journal of Nanchang University:Medical Sciences
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  • 1冯献启,邹萍.内质网应激反应性凋亡途径研究进展[J].国外医学(肿瘤学分册),2004,31(10):726-730. 被引量:15
  • 2Ferri K F, Kroemer G. Organelle-specific initiation of cell death pathways. Nat Cell Biol, 2001, 3: E255-E263.
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  • 6Rao R V, Hermel E, Castro-Obregon S, et al. Coupling endoplasmic reticulum stress to the cell death program. Mechanism of caspase activation. J Biol Chem, 2001, 276: 33869-33874.
  • 7Xie Q, Khaoustov V I, Chung C C, et al. Effect of tauroursodeoxycholic acid on endoplasmic reticulum stress-induced caspase-12 activation. Hepatology, 2002, 36: 592-601.
  • 8PrachasilchaiW, Sonoda H, Yokota-Ikeda N, et al. A protective role of unfolded protein response in mouse ischemic acute kidney injury. Eur J Pharmacol, 2008, 592:138-145.
  • 9Izuhara Y, Nangaku M, Takizawa S, et al. A novel class of advanced glycation inhibitors ameliorates renal and cardiovascular damage in experimental rat models. Nephrol Dial Transplant, 2008, 23: 497-509.
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