ArticleFrontiers in pharmacology2026
Multi-omics analysis reveals
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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
2 citing papers in PubMed.
- Integrated Network Pharmacology and Single-Cell Transcriptomics Reveal Transketolase as a Potential Target for the DanShen-DaHuang Herb Pair in Acute Kidney Injury.International journal of molecular sciences · 2026Article
- Wulingsan alleviates cisplatin-induced acute kidney injury and inhibits renal tubular epithelial cell apoptosis in association with the CaSR/CaMKKβ/AMPK pathway.Frontiers in pharmacology · 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
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute Kidney Injury (AKI) is a critical clinical syndrome with high morbidity and mortality, yet effective therapeutic agents are lacking. The Objective: This study aimed to evaluate the nephroprotective effects of the R-S combination on cisplatin-induced AKI and to elucidate its underlying mechanisms through integrated multi-omics analyses. Methods: Male C57BL/6 mice were randomly divided into five groups: Control group (Control), AKI model group (Model), Results: R-S treatment significantly improved renal function, lowering Cr and BUN, and attenuated renal histopathological injury. It also reduced oxidative stress and inflammation, elevating SOD and GSH, while decreasing IL-1β and TNF-α. Gut microbiota analysis showed that R-S restored microbial diversity, suppressed Escherichia-Shigella, and promoted Lachnospiraceae_NK4A136_group. Metabolomics identified 1237 differential metabolites, with enrichment in linoleic acid metabolism. Transcriptomics revealed 3530 differentially expressed genes, primarily associated with the MAPK signaling pathway. Molecular validation confirmed that R-S downregulated the mRNA expression of IL-1β, IL-6, TNF-α, MAPK 14, MAPK 8, NFKB 1, FOS, and JUN, and suppressed the phosphorylation of p38 MAPK, JNK, and NF-κB p65. Conclusion: The R-S combination alleviates cisplatin-induced AKI by modulating the gut microbiota, regulating metabolic profiles, and suppressing the MAPK signaling axis. This study provides a holistic, multi-omics perspective on the mechanisms of R-S, supporting its potential as a therapeutic agent for AKI.
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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 Socratic graph.