ArticleScientific reports2024
Metabolomic and transcriptomic insights into the mechanisms of renal ischemia-reperfusion injury progression.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences.Journal of translational medicine · 2026Review
- Multi-Omics Analysis Identifies Tryptophan Metabolism and Glycolysis as Potential Pathways Involved in the Protective Effects of Tormentic Acid Against Metabolic Associated Fatty Liver Disease.Pharmacology research & perspectives · 2026Article
- Interplay between ischemia-reperfusion and metabolic reprogramming.Apoptosis : an international journal on programmed cell death · 2026Review
- High-Resolution Spatiotemporal Mapping of Cerebral Metabolism During Middle-Cerebral-Artery Occlusion/Reperfusion Progression: Preliminary Insights.Biomolecules · 2025Article
- Sinapic acid alleviates renal ischemia-reperfusion injury by regulating oxidative stress, apoptosis, and inflammation.Turkish journal of medical sciences · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Renal ischemia-reperfusion injury (IRI) is an important cause of acute kidney injury (AKI). However, the pathophysiological changes and mechanisms during IRI-AKI progression remain unclear. This study aims toinvestigate the potential mechanisms in the progression of IRI-AKI by integrating metabolomics and transcriptomics data, providing a reference for the subsequent identification of biomarkers and therapeutic targets. IRI-AKI rat models with 30 min of ischemia and 24-72 h of reperfusion surgery simulating the progression of AKI were established. Compared to the control group underwent sham surgery (NC group), most of the differentially expressed metabolites (DEMs) in IRI-AKI 24 h and IRI-AKI 72 h decreased, mainly including amino acids, organic acids, and carnitines. Additionally, we found that DEMs were mainly enriched in amino acid-related pathways, among which valine, leucine, and isoleucine biosynthesis were dramatically altered in all comparisons. Transcriptomics revealed that differentially expressed genes (DEGs) were primarily involved in amino acid, lipid, and fatty acid metabolism. By integrating metabolomics and transcriptomics, we found valine, leucine, and isoleucine biosynthesis play key roles in IRI-AKI development. Our findings concluded that valine, leucine, and isoleucine pathways are hubs that potentially connect transcriptomes to metabolomes, providing new insights regarding the pathogenesis of IRI-AKI and its potential biomarkers and therapeutic strategies.
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Registered trials
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