Lin Fangming, Wang Zhao V, Hill Joseph A
Department of Pediatrics; Columbia University College of Physicians and Surgeons; and.
Department of Internal Medicine; University of Texas Southwestern Medical Center; Dallas, TX USA.
Autophagy. 2014 Apr;10(4):691-3. doi: 10.4161/auto.27749. Epub 2014 Jan 14.
Ischemic injury to the kidneys is a prevalent clinical problem, contributing importantly to chronic kidney disease. Yet, underlying molecular mechanisms are elusive. To address the possible role of autophagy, we engineered a novel strain of mice harboring a ubiquitously expressed CAG-RFP-EGFP-LC3 transgene. Using this tool, we examined the post-ischemic kidney and detailed the dynamics of renal tubular epithelial autophagy. In addition, we defined the role of MTOR in the resolution of autophagy during epithelial survival and kidney repair.
肾脏缺血性损伤是一个普遍存在的临床问题,对慢性肾脏病的发生发展起着重要作用。然而,其潜在的分子机制尚不清楚。为了探讨自噬的可能作用,我们构建了一种新型小鼠品系,该品系携带一个在全身广泛表达的CAG-RFP-EGFP-LC3转基因。利用这一工具,我们对缺血后的肾脏进行了研究,并详细阐述了肾小管上皮细胞自噬的动态变化。此外,我们还确定了mTOR在上皮细胞存活和肾脏修复过程中自噬消退中的作用。