Summary of Study ST003042
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 PR001893. The data can be accessed directly via it's Project DOI: 10.21228/M81F0P 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.
| Study ID | ST003042 |
| Study Title | The metabolomic resetting effect of DY131 in cisplatin-induced AKI |
| Study Type | MS |
| Study Summary | LC-MS/MS analyses were performed using renal tissues from cisplatin-induced AKI mice with or without DY131 treatment. The data revealed that DY131 alleviated cisplatin-induced mitochondrial dysfunction and energy metabolism disorder, as well as multiple metabolic disorders. |
| Institute | Children's Hospital of Nanjing Medical University |
| Department | Department of Nephrology, State Key Laboratory of Reproductive Medicine |
| Laboratory | Nanjing Key Lab of Pediatrics, Jiangsu Key Laboratory of Pediatrics |
| Last Name | Lu |
| First Name | Lingling |
| Address | Guangzhou Road 72, Nanjing, Jiangsu, 210000, China |
| lulingling89tara@163.com | |
| Phone | 0086-25-8311-7435 |
| Submit Date | 2023-12-21 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | mzXML |
| Analysis Type Detail | LC-MS |
| Release Date | 2024-02-08 |
| Release Version | 1 |
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Project:
| Project ID: | PR001893 |
| Project DOI: | doi: 10.21228/M81F0P |
| Project Title: | The metabolomic resetting effect of DY131 in cisplatin-induced AKI |
| Project Type: | MS quantitative analysis |
| Project Summary: | Acute kidney injury (AKI) remains a challenge in clinical practice, and mitochondrial injury is a hallmark of AKI independent of the exact aetiology. ERRĪ³ is a member of orphan nuclear receptors which plays a regulatory role in mitochondrial biosynthesis, energy metabolism, oxidative stress, cell apoptosis, inflammation, and especially metabolic pathways. Here we investigate the role of pharmacological agonist of ERRĪ³, DY131, in AKI mice induced by cisplatin, IR and LPS. DY131 ameliorated renal function, tubular injury, cell apoptosis and inflammation in AKI mice with multiple causes. Furthermore, we performed LC-MS/MS analyses using renal tissues from cisplatin-induced AKI mice with or without DY131 treatment. Strikingly, the data revealed that DY131 alleviated cisplatin-induced mitochondrial dysfunction and energy metabolism disorder, as well as multiple metabolic disorders. Taken together, the findings highlighted the protective effect of DY131 on AKI probably via improving mitochondrial function and energy metabolism. |
| Institute: | Children's Hospital of Nanjing Medical University |
| Department: | Department of Nephrology, State Key Laboratory of Reproductive Medicine |
| Laboratory: | Nanjing Key Lab of Pediatrics, Jiangsu Key Laboratory of Pediatrics |
| Last Name: | Lu |
| First Name: | Lingling |
| Address: | Guangzhou Road 72, Nanjing, Jiangsu, 210000, China |
| Email: | lulingling89tara@163.com |
| Phone: | 0086-25-8311-7435 |
