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Augmenter of liver regeneration promotes mitochondrial biogenesis in renal ischemia–reperfusion injury

Overview of attention for article published in Apoptosis, September 2018
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Title
Augmenter of liver regeneration promotes mitochondrial biogenesis in renal ischemia–reperfusion injury
Published in
Apoptosis, September 2018
DOI 10.1007/s10495-018-1487-2
Pubmed ID
Authors

Li-li Huang, Rui-ting Long, Gui-ping Jiang, Xiao Jiang, Hang Sun, Hui Guo, Xiao-hui Liao

Abstract

Mitochondria are the center of energy metabolism in the cell and the preferential target of various toxicants and ischemic injury. Renal ischemia-reperfusion (I/R) injury triggers proximal tubule injury and the mitochondria are believed to be the primary subcellular target of I/R injury. The promotion of mitochondrial biogenesis (MB) is critical for the prevention I/R injury. The results of our previous study showed that augmenter of liver regeneration (ALR) has anti-apoptotic and anti-oxidant functions. However, the modulatory mechanism of ALR remains unclear and warrants further investigation. To gain further insight into the role of ALR in MB, human kidney (HK)-2 cells were treated with lentiviruses carrying ALR short interfering RNA (siRNA) and a model of hypoxia reoxygenation (H/R) injury in vitro was created. We observed that knockdown of ALR promoted apoptosis of renal tubular cells and aggravated mitochondrial injury, as evidenced by the decrease in the mitochondrial respiratory proteins adenosine triphosphate (ATP) synthase subunit β, cytochrome c oxidase subunit 1, and nicotinamide adenine dinucleotide dehydrogenase (ubiquinone) beta subcomplex 8. Meanwhile, the production of reactive oxygen species was increased and ATP levels were decreased significantly in HK-2 cells, as compared with the siRNA/control group (p < 0.05). In addition, the mitochondrial DNA copy number and membrane potential were markedly decreased. Furthermore, critical transcriptional regulators of MB (i.e., peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, mitochondrial transcription factor A, sirtuin-1, and nuclear respiratory factor-1) were depleted in the siRNA/ALR group. Taken together, these findings unveil essential roles of ALR in the inhibition of renal tubular cell apoptosis and attenuation of mitochondrial dysfunction by promoting MB in AKI.

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Mendeley readers

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Geographical breakdown

Country Count As %
Unknown 11 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 2 18%
Other 1 9%
Student > Bachelor 1 9%
Student > Ph. D. Student 1 9%
Professor 1 9%
Other 2 18%
Unknown 3 27%
Readers by discipline Count As %
Medicine and Dentistry 2 18%
Pharmacology, Toxicology and Pharmaceutical Science 1 9%
Business, Management and Accounting 1 9%
Biochemistry, Genetics and Molecular Biology 1 9%
Physics and Astronomy 1 9%
Other 1 9%
Unknown 4 36%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 28 September 2018.
All research outputs
#20,535,139
of 23,105,443 outputs
Outputs from Apoptosis
#634
of 811 outputs
Outputs of similar age
#296,864
of 341,556 outputs
Outputs of similar age from Apoptosis
#7
of 13 outputs
Altmetric has tracked 23,105,443 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 811 research outputs from this source. They receive a mean Attention Score of 3.6. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 13 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.