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摘要
Linkermann et al. provide the first evidence for a possible biochemical mechanism of necrotic kidney cell death associated with renal ischemia/reperfusion-induced acute kidney injury. The mechanisms of several pathways resulting in programmed necrosis were recently elucidated and rely on receptor-interacting protein kinases 1 and 3. Using an inhibitor of one of these kinases, Linkermann et al. were able to ameliorate functional and morphologic kidney damage after ischemia/reperfusion. Kidney International (2012) 81, 720-721. doi:10.1038/ki.2011.495
- 出版日期2012-4
