Summary of Study ST001747

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001119. The data can be accessed directly via it's Project DOI: 10.21228/M82D8P This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST001747
Study TitleLung metabolomics after ischemic acute kidney injury reveals increased oxidative stress, altered energy production, and ATP depletion
Study SummaryAcute kidney injury (AKI) is a complex disease associated with increased mortality that may be due to deleterious distant organ effects. AKI associated with respiratory complications, in particular, has a poor outcome. In murine models, AKI is characterized by increased circulating cytokines, lung chemokine upregulation, and neutrophilic infiltration, similar to other causes of indirect acute lung injury (ALI)(e.g., sepsis). Many causes of lung inflammation are associated with a lung metabolic profile characterized by increased oxidative stress, a shift towards the use of other forms of energy production, and/or a depleted energy state. To our knowledge, there are no studies that have evaluated pulmonary energy production and metabolism after AKI. We hypothesized that based on the parallels between inflammatory acute lung injury and AKI-mediated lung injury, a similar metabolic profile would be observed. Lung metabolomics and ATP levels were assessed 4 hours, 24 hours, and 7 days after ischemic AKI in mice. Numerous novel findings regarding the effect of AKI on the lung were observed including 1) increased oxidative stress, 2) a shift toward alternate methods of energy production, and 3) depleted levels of ATP. The findings in this report bring to light novel characteristics of AKI-mediated lung injury and provide new leads into the mechanisms by which AKI in patients predisposes to pulmonary complications.
Institute
University of Colorado Anschutz Medical Campus
Last NameHaines
First NameJulie
Address12801 E 17th Ave, Room 1303
Emailjulie.haines@cuanschutz.edu
Phone3037243339
Submit Date2021-04-15
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2021-05-04
Release Version1
Julie Haines Julie Haines
https://dx.doi.org/10.21228/M82D8P
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id group time point
SA163433534AKI 24h
SA163434531AKI 24h
SA163435522AKI 24h
SA163436546AKI 24h
SA163437525AKI 24h
SA163438528AKI 24h
SA163439549AKI 24h
SA163440558AKI 24h
SA163441555AKI 24h
SA163442552AKI 24h
SA163443517AKI 4h
SA163444515AKI 4h
SA163445513AKI 4h
SA163446519AKI 4h
SA163447543AKI 4h
SA163448511AKI 4h
SA163449545AKI 4h
SA163450539AKI 4h
SA163451537AKI 4h
SA163452541AKI 4h
SA163453503AKI 7d
SA163454505AKI 7d
SA163455501AKI 7d
SA163456496AKI 7d
SA163457500AKI 7d
SA163458498AKI 7d
SA163459529normal 24h
SA163460523normal 24h
SA163461526normal 24h
SA163462556normal 24h
SA163463559normal 24h
SA163464553normal 24h
SA163465550normal 24h
SA163466532normal 24h
SA163467535normal 24h
SA163468547normal 24h
SA163469554sham 24h
SA163470560sham 24h
SA163471551sham 24h
SA163472557sham 24h
SA163473521sham 24h
SA163474548sham 24h
SA163475527sham 24h
SA163476524sham 24h
SA163477530sham 24h
SA163478533sham 24h
SA163479518sham 4h
SA163480520sham 4h
SA163481512sham 4h
SA163482536sham 4h
SA163483514sham 4h
SA163484540sham 4h
SA163485538sham 4h
SA163486544sham 4h
SA163487516sham 4h
SA163488542sham 4h
SA163489493sham 7d
SA163490497sham 7d
SA163491508sham 7d
SA163492510sham 7d
SA163493504sham 7d
SA163494502sham 7d
SA163495495sham 7d
SA163496499sham 7d
SA163497491sham 7d
Showing results 1 to 65 of 65
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