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HIV-1 Vpr 激活肾小管上皮细胞中的 DNA 损伤反应。

HIV-1 Vpr activates the DNA damage response in renal tubule epithelial cells.

机构信息

Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA.

出版信息

AIDS. 2009 Sep 24;23(15):2054-6. doi: 10.1097/QAD.0b013e32833088a0.

Abstract

HIV-associated nephropathy (HIVAN) is a major cause of HIV-related morbidity and mortality. Pathogenesis involves direct infection of the glomerular and tubular epithelial cells leading to characteristic disorder. Recently, we have shown that HIV-1 Vpr causes hypertrophy, hyperploidy, and apoptosis. Here, we report that Vpr activates the DNA damage response resulting in the observed renal phenotype. Renal sections from the HIVAN transgenic mouse model and human biopsies both show an abundant DNA damage response.

摘要

HIV 相关性肾病(HIVAN)是导致 HIV 相关发病率和死亡率的主要原因之一。发病机制涉及肾小球和肾小管上皮细胞的直接感染,导致特征性的紊乱。最近,我们已经证明 HIV-1 Vpr 会导致肥大、多倍体形成和细胞凋亡。在这里,我们报告 Vpr 激活了 DNA 损伤反应,从而导致了所观察到的肾脏表型。HIVAN 转基因小鼠模型和人类活检的肾组织切片均显示出丰富的 DNA 损伤反应。

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