ArticleScientific reports2026
Metabolomic assessment reveals depletion of amino acids and energy metabolites in skeletal muscle after ischemic acute kidney injury in mice.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Integrated network pharmacology and serum metabolomics to reveal the protective mechanism of methanolic extract of BaiYangJie on cisplatin-induced acute kidney injury in mice.Experimental and therapeutic medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Acute kidney injury (AKI) is a systemic catabolic condition that affects multiple organs. Clinically, AKI has been associated with muscle wasting, weakness, and delayed functional recovery. The underlying biochemical mechanisms driving these changes are not well understood. Ischemic AKI was induced in 8-10-week-old male C57BL/6 mice. Untargeted metabolomics on gastrocnemius samples were performed via ultra-high performance liquid chromatography-mass spectrometry at 24 h and 72 h after AKI. Of the 175 annotated analytes identified, 72 were significantly affected at 24 h with the majority of these metabolites being depleted in AKI compared to controls. Key depleted metabolites included multiple amino acids, glutathione and its precursors, and other energy-related substrates. Integration with our previously published metabolomics data in the kidney, liver, heart, and plasma highlights shared metabolic pathways across these organs, particularly reflected in arginine metabolism and the urea cycle, alanine/aspartate/glutamate metabolism, and glutathione/redox balance. This is the first study to characterize the metabolic profile of skeletal muscle after ischemic AKI in a murine model. Our data deepen the understanding of AKI as a systemic metabolic disease, underscoring the need to further understand the effects of AKI on skeletal muscle and opening potential avenues for therapeutic strategies to improve outcomes after AKI.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.