ArticleVirulence2026
Integrated transcriptomic, molecular docking, and mendelian randomization analysis reveal a microbial-propionate-JUN pathway in renal ischemia-reperfusion injury.
Article in Virulence, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Article
- Microbiota-associated metabolic networks in gut-kidney communication and renal immune regulation: mechanisms and therapeutic potential.Frontiers in microbiology · 2026Review
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Authors and funding
7 authors.
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Abstract
Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury and is characterized by oxidative stress, immune cell infiltration, and inflammatory signaling activation. Although gut microbiota and their metabolites, especially short-chain fatty acids, are involved in systemic immune regulation, their role in renal IRI remains unclear. Here, we integrated transcriptomic analysis, gut-derived metabolite target prediction, molecular docking, and Mendelian randomization (MR) to explore potential microbiota-metabolite-host regulatory mechanisms in renal IRI. We identified 32 target genes of gut-derived metabolites using the gutMGene, Similarity Ensemble Approach, and SwissTargetPrediction databases. In two renal IRI datasets (GSE126805 and GSE90861), 263 and 641 differentially expressed genes were identified, respectively, and hub genes were mainly enriched in the TNF and IL-17 signaling pathways. Among them, JUN was identified as a key hub linking gut microbiota-associated metabolites to renal inflammatory signaling. MR analysis showed that
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