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Qingqing Wei

Researcher at Georgia Regents University

Publications -  57
Citations -  4513

Qingqing Wei is an academic researcher from Georgia Regents University. The author has contributed to research in topics: Kidney & Apoptosis. The author has an hindex of 27, co-authored 47 publications receiving 3730 citations. Previous affiliations of Qingqing Wei include Chinese Academy of Sciences & Veterans Health Administration.

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Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models

TL;DR: In vivo analysis revealed that mitochondrial fragmentation also occurred in proximal tubular cells in mice during renal ischemia/reperfusion and cisplatin-induced nephrotoxicity, and was identified as what is believed to be a novel mechanism contributing to mitochondrial damage and apoptosis in vivo in mouse models of disease.
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Autophagy in proximal tubules protects against acute kidney injury

TL;DR: The results establish a renoprotective role of tubular cell autophagy in acute kidney injury where it may interfere with cell killing mechanisms and establish a renal proximal tubule-specific Autophagy-related gene 7 knockout mouse model.
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Bak regulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins

TL;DR: A previously unrecognized function of Bak is uncovered in the regulation of mitochondrial morphological dynamics during apoptosis, by this function, Bak may collaborate with Bax to permeabilize the outer membrane of mitochondria, unleashing the apoptotic cascade.
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Autophagy is cytoprotective during cisplatin injury of renal proximal tubular cells

TL;DR: In this paper, the authors found that administration of cisplatin induced the formation of autophagic vesicles and autophagosomes in mouse kidneys, and this was partially suppressed by the p53 inhibitor pifithrin-α.
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Mouse model of ischemic acute kidney injury: technical notes and tricks

TL;DR: A detailed protocol of the mouse model of bilateral renal ischemia-reperfusion is described and the technical issues that account for the variability of this model are discussed and relevant solutions are offered, which may help other investigators to establish a well-controlled, reliable animal model of ischemic AKI.