Transcriptome sequencing of liver injury models
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ABSTRACT:
PROVIDER: PRJNA1274471 | ENA |
REPOSITORIES: ENA
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2025-06-30 | GSE299455 | GEO
Project description:INTRODUCTION Ischemia and reperfusion injury (IRI)-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest 1. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery 1. IRI, one of the biggest challenges for organ transplantation, continues to be a vital source of morbidity among recipients, especially in liver transplantation 2. With the enlarging shortage of available donor livers, the increased use of extended criteria donor grafts further increases IRI, adversely affecting both short-term and long-term outcomes of graft and patient survival 3. Numerous studies have investigated the benefits of pharmacological, heat shock, and ischemic preconditioning interventions aimed at decreasing liver IRI 4. However, the benefit was limited. Our center has been making great effort in conquering IRI and have developed a novel surgical technique called ischemia-free liver transplantation 5. It is an ultimate method to overcome IRI in liver transplantation, but there is still a long way to popularize it. As a result, it is still of great significance to study IRI and identify the core genes in the process and the underlying mechanism. Comprehensive bioinformatics analysis has been increasingly important as a method to study various pathological and physiological condition 6. By enrolling multiple omics or combining different types of omics, comprehensive bioinformatics analysis was able to recognize key factors that could have potentially pathogenic impact such as gene expression, protein function, and downstream pathways. With the rapid development of high-throughput sequencing technologies, several transcriptomic datasets on IRI of liver transplantation have become available in the Gene Expression Omnibus (GEO) database. Herein, we recruited 3 GEO datasets to conduct comprehensive analysis with the GEO dataset from our center. Moreover, we performed the first proteome of liver tissues to study liver IRI. Then the transcriptome and proteome were used for combined analysis to reveal key factors in liver IRI.
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Project description:<p>The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) has established the Drug-Induced Liver Injury Network (DILIN) to collect and analyze cases of severe liver injury caused by prescription drugs, over-the-counter drugs, and alternative medicines, such as herbal products and supplements.</p>
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Project description:<p>Tetracycline antibiotics (TETs) cause hepatotoxicity via gut-liver axis disruption and oxidative stress. This study evaluated whether formononetin (FMN), a natural isoflavone, alleviates TET-induced liver injury through microbiota-metabolite-transcriptome coordination. Using network toxicology and pharmacology, we predicted key targets and pathways involved. A mouse model of TET-induced injury (150 mg/kg, 3 days) was treated with FMN (50 or 100 mg/kg) for 14 days. Multi-omics analyses revealed that FMN attenuated hepatic steatosis, reduced ALT/AST levels, enhanced gut microbial diversity (enriched Limosilactobacillus), and restored intestinal barrier integrity. Mechanistically, FMN activated the Nrf2/HO-1 antioxidant pathway, modulated PPARα/CYP2E1-dependent lipid metabolism, and inhibited ferroptosis. FMN demonstrates multi-target hepatoprotection by coordinating microbiota restoration, oxidative stress reduction, and metabolic reprogramming, supporting its potential as a dietary intervention against antibiotic-related liver damage.</p>
2025-10-14 | MTBLS13138 | MetaboLights
Project description:<p>Tetracycline antibiotics (TETs) cause hepatotoxicity via gut-liver axis disruption and oxidative stress. This study evaluated whether formononetin (FMN), a natural isoflavone, alleviates TET-induced liver injury through microbiota-metabolite-transcriptome coordination. Using network toxicology and pharmacology, we predicted key targets and pathways involved. A mouse model of TET-induced injury (150 mg/kg, 3 days) was treated with FMN (50 or 100 mg/kg) for 14 days. Multi-omics analyses revealed that FMN attenuated hepatic steatosis, reduced ALT/AST levels, enhanced gut microbial diversity (enriched Limosilactobacillus), and restored intestinal barrier integrity. Mechanistically, FMN activated the Nrf2/HO-1 antioxidant pathway, modulated PPARα/CYP2E1-dependent lipid metabolism, and inhibited ferroptosis. FMN demonstrates multi-target hepatoprotection by coordinating microbiota restoration, oxidative stress reduction, and metabolic reprogramming, supporting its potential as a dietary intervention against antibiotic-related liver damage.</p>
2025-10-17 | MTBLS13161 | MetaboLights
Project description:To understand the roles of ferroptosis in subsequent acute kidney injury (AKI) following hepatic ischemia-reperfusion injury (hIRI) in steatosis livers. The hIRI was induced in mice fed either a high-fat, high-sucrose diet (HFD) or a normal diet (ND) to mimic the AKI commonly observed clinically after fatty liver transplantation. RNA sequencing was conducted to investigate the underlying mechanisms. We found that apoptosis and inflammation are the prominent kidney injury mechanisms following fatty liver IRI. Although ferroptosis may not be directly involved in the renal injury, anti-ferroptosis intervention mitigates AKI, supporting the concept that ferroptosis-mediated liver injury may serve as the primary upstream trigger in this context.
2025-11-21 | GSE309904 | GEO
Project description:We previously showed that severe liver diseases are characterized by expansion of liver progenitor cells (LPC), which correlates with disease severity. However, the origin and role of LPC in liver physiology and in the hepatic response to injury remains a contentious topic. We have now used genetic lineage tracing of Hnf1β-expressing biliary duct cells to assess their contribution to LPC expansion and hepatocyte generation during normal liver homeostasis, and following different types of liver injury. We found that ductular reaction cells in human cirrhotic livers express HNF1β. However, HNF1β expression was not present in newly generated EpCAM-positive hepatocytes. Using a tamoxifen-inducible Hnf1βCreER/R26RYFP/LacZ mouse, we show that there is no contribution of the biliary epithelium to hepatocyte turnover during liver homeostasis in healthy mice. Moreover, after loss of liver mass, Hnf1β+ LPC did not contribute to hepatocyte regeneration. We also assessed the contribution of Hnf1β+ cells following acute and repeated liver injury. All animal models showed expansion of LPC, as assessed by immunostaining and gene expression profile of sorted YFP-positive cells. A contribution of Hnf1β+ LPC to hepatocyte generation was not detected in animal models of liver injury with preserved hepatocyte regenerative potential such as acute acetaminophen, carbon tetrachloride injury, or chronic diethoxycarbonyl-1,4-dihydro-collidin (DDC)-diet. However, in mice fed with choline-deficient ethionine-supplemented (CDE)-diet, which causes profound hepatocyte damage and arrest, a small number of hepatocytes were derived from Hnf1β+ cells. Conclusion: Hnf1β+ cells do not participate in hepatocyte turnover in the healthy liver or during liver regeneration after partial hepatectomy. After liver injury, LPC arise from the biliary duct epithelium, which gives rise to a limited number of hepatocytes only when hepatocyte regeneration is compromised. Transcriptomic profile using MoGeneST-2.0 chip from 3 samples of YFP+ CDE, 3 samples of YFP+ DDC, 2 samples of YFP+ UTR and 3 samples YFP-
2016-07-03 | E-GEOD-51389 | biostudies-arrayexpress