ArticleAnnals of translational medicine2022
Transcriptomic analysis and laboratory experiments reveal potential critical genes and regulatory mechanisms in sepsis-associated acute kidney injury.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- METTL3/IGF2BP1 Axis Orchestrates m6A-Dependent NCAM1 Preservation to Combat Age-Related Cognitive Decline.Cells · 2026Article
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Inhibition of iron overload and ferroptosis attenuates sepsis-induced myocardial injury in mice through STAT3/Lcn2 pathway.Journal of cardiothoracic surgery · 2026Article
- JAK2/STAT3-dependent regulation of MDM4/MDM2-p53 signaling in methotrexate-induced ferroptosis and nephrotoxicity.Archives of pharmacal research · 2026Article
- Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury.International journal of molecular sciences · 2026Review
- Dexmedetomidine alleviates sepsis-associated acute kidney injury by inhibiting renal tubular ferroptosis via JNK/MAPK-LCN2 pathway.European journal of medical research · 2026Article
- Unravelling Ferroptosis in Sepsis: A Comprehensive Integrative Transcriptomic Analysis Across Age and Disease Severity.Bioinformatics and biology insights · 2026Article
- Diagnostic Value and Mechanism of Action of LINC00641 in Sepsis-Associated Acute Kidney Injury.Journal of inflammation research · 2026Article
- Protective Effects of Cyclosporin H Against Sepsis-Induced Acute Kidney Injury via Modulation of Fpr1 Signaling and Inhibiting Pyroptosis.Research and reports in urology · 2026Article
- C7ORF41 Alleviates Ferroptosis Via the Keap1/Nrf2/HO-1 Axis in Endotoxin-Associated Acute Kidney Injury.Inflammation · 2025Article
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- METTL14 alleviates sepsis-induced acute kidney injury by targeting Hmox1-mediated ferroptosis through m6A modification.Journal of molecular histology · 2025Article
- Molecular insights and clinical implications of DNA methylation in sepsis-associated acute kidney injury: a narrative review.BMC nephrology · 2025Review
- Novel insights into the molecular mechanisms of sepsis-associated acute kidney injury: an integrative study of GBP2, PSMB8, PSMB9 genes and immune microenvironment characteristics.BMC nephrology · 2025Article
- The role of ferroptosis in acute kidney injury: mechanisms and potential therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Methyltransferase-like 14 promotes ferroptosis in sepsis-induced acute kidney injury via increasing the m6A methylation modification of LPCAT3.Molecular genetics and genomics : MGG · 2025Article
- The role of N6-methyladenosine (mPeerJ · 2025Review
- Machine learning-based transcriptmics analysis revealsFrontiers in pharmacology · 2025Article
- Molecular mechanism of ALKBH5-mediated m6A demethylation regulating lipopolysaccharide-induced epithelial-mesenchymal transition in sepsis-induced acute kidney injury.The Kaohsiung journal of medical sciences · 2024Article
- Regulation of renal ischemia-reperfusion injury and tubular epithelial cell ferroptosis by pparγ m6a methylation: mechanisms and therapeutic implications.Biology direct · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sepsis-associated acute kidney injury (SA-AKI) is one of the most frequent and serious complications of sepsis. However, the transcriptional regulatory network of the pathophysiological mechanism of the kidney has not been revealed. This study identified new mechanisms in SA-AKI using bioinformatics analyses and laboratory-based experiments. Methods: We performed transcriptomic profiling of mouse kidneys after cecal ligation and puncture (CLP) to mimic clinical sepsis. RNA from kidney samples from the CLP and control groups was isolated and analyzed using bulk messenger RNA (mRNA)-seq. Differentially expressed genes (DEGs) between the two groups were identified, and GO, KEGG and GSEA pathway enrichment analyses were performed. The protein-protein interaction (PPI) network of DEGs and hub genes was analyzed. The hub genes were verified using quantitative real-time polymerase chain reaction (qPCR) or Western blotting. The interaction network, targeted microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) of hub genes were predicted, and the critical miRNA-hub gene regulatory axis was verified using qPCR, Western blotting, malondialdehyde (MDA) determination and flow cytometry. Correlation analyses of N6-adenosine methylation (m6A) RNA methylation regulators and hub genes and m6A modification analysis were performed. Results: A total of 4,754 DEGs were identified between the two groups using high-throughput sequencing. The pathways in which DEGs were enriched included ferroptosis (the highest enrichment score), apoptosis, and the PI3K-Akt, NF-kappa B and IL-17 signaling pathways. Seven ( Conclusions: The findings of this study provide new insights into the mechanism regulating the occurrence and progression of SA-AKI. The mmu-miR-7212-5p-Hmox1 axis in ferroptosis and m6A RNA methylation regulators may have potential clinical significance for the future treatment of SA-AKI. The datasets generated for this study can be found in the repository of the GEO database (Series number: GSE186822).
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