Summary of Study ST002989

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 PR001861. The data can be accessed directly via it's Project DOI: 10.21228/M85B0W This work is supported by NIH grant, U2C- DK119886.

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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 IDST002989
Study TitleTargeting NPM1 Epigenetically Promotes Post-infarction Cardiac Repair by Reprogramming Reparative Macrophage Metabolism
Study SummaryReparative macrophages play a crucial role in limiting excessive fibrosis and promoting cardiac repair after myocardial infarction (MI), highlighting the significance of enhancing their reparative phenotype for wound healing. Metabolic adaptation orchestrates the phenotypic transition of macrophages; however, the precise mechanisms governing metabolic reprogramming of cardiac reparative macrophages remain poorly understood. In this study, we investigated the role of Nucleophosmin 1 (NPM1) in the metabolic and phenotypic shift of cardiac macrophages in the context of MI, and explored the effect of targeting NPM1 for ischemic tissue repair.
Institute
Renji Hospital, Shanghai Jiao Tong University School of Medicine
Last NameZhan
First NameZhenzhen
Address160 Pujian Road, Shanghai, Shanghai, 200127, China
Emailzhanzz2022@sjtu.edu.cn
Phone86-21-61569249
Submit Date2023-11-23
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2024-03-20
Release Version1
Zhenzhen Zhan Zhenzhen Zhan
https://dx.doi.org/10.21228/M85B0W
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Treatment:

Treatment ID:TR003111
Treatment Summary:mouse bone marrow cells were flushed out from mouse femurs using RPMI 1640 and cultured in a complete RPMI 1640 medium (added with 10% fetal bovine serum and 1% penicillin/streptomycin) supplemented with 20 ng/ml M-CSF for 7 days to generate mature BMDMs. BMDMs were stimulated with 20 ng/ml IL-4 for 12 h to induce a reparative phenotype.
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