Development of a novel non-invasive biomarker panel for hepatic fibrosis in individuals with MASLD
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ABSTRACT:
PROVIDER: PRJNA1005170 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25630200_1.fastq.gz | Fastqsanger.gz | |||
| SRR25630200_2.fastq.gz | Fastqsanger.gz | |||
| SRR25630201_1.fastq.gz | Fastqsanger.gz | |||
| SRR25630201_2.fastq.gz | Fastqsanger.gz | |||
| SRR25630202_1.fastq.gz | Fastqsanger.gz |
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Project description:- Background & Aims: Considering the escalating prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) and MASLD-related fibrosis, accurate non-invasive biomarkers for diagnosis and staging of fibrosis are urgently needed. This study Aims to develop a blood-based biomarker panel for fibrosis detection in individuals with MASLD. - Approach & Results: Using a translational diet-induced LDLr-/-.Leiden MASLD mouse model, candidate biomarkers were identified focused on the mechanism of collagen deposition, by integrating hepatic gene expression and new extracellular matrix deposition, as detected by dynamic D2O-labeling. To translate these findings to humans, gene expression profiles and biomarkers were analyzed in liver biopsies and serum samples from 67 individuals with histologically characterized MASLD and variable degrees of fibrosis. This led to the selection of three biomarkers for a blood-based fibrosis biomarker panel: IGFBP7, SSc5D and Sema4D. The accuracy of the biomarker panel was tested in a separate cohort of 128 individuals with histologically characterized MASLD across different stages of fibrosis. A Light Gradient Boosting Machine (LGBM) model was applied to predict fibrosis stage in MASLD (F0/F1: AUC = 0.90; F2: AUC = 0.91; F3/F4: AUC = 0.87). - Conclusion & Discussion: Using a translational Approach to identify collagen turnover related proteins indicative of fibrosis, we developed an accurate blood-based biomarker panel to detect and stage hepatic fibrosis in individuals with MASLD.
2024-05-17 | GSE240729 | GEO
Project description:Purpose: Gastric cancer (GC) is one of the most common causes of cancer deaths worldwide; however, reliable and non-invasive screening methods for GC are not established. Therefore, we conducted this study to develop a biomarker for GC detection, consisting of urinary microRNAs (miRNAs). Experimental Design: We matched 306 participants by age and sex (153 pairs consisting of patients with GC and healthy controls [HCs]), then randomly divided them across three groups: (1) the discovery cohort (4 pairs); (2) the training cohort (95 pairs); (3) the validation cohort (54 pairs). Moreover, 64 participants (32 pairs) with serum samples were also enrolled in the serum cohort. Result: There were 22 urinary miRNAs with significantly aberrant expressions between the two groups in the discovery cohort. Upon multivariate analysis of the training cohort, urinary expression levels of miR-6807-5p and miR-6856-5p were significantly independent biomarkers for diagnosis of GC, in addition to Helicobacter pylori (H. pylori) status. A diagnostic panel that combined the aberrant miRNAs and H. pylori status distinguished between HC and GC samples with an area under the curve (AUC) = 0.736. In the validation cohort, urinary miR-6807-5p and miR-6856-5p showed significantly higher expression levels in the GC group, and the combination biomarker panel of miR-6807-5p, miR-6856-5p, and H. pylori status also showed excellent performance (AUC = 0.885). In addition, serum levels of miR-6807-5p and miR-6856-5p were significantly higher in the GC group. Conclusion: This novel biomarker panel enables early and non-invasive detection of GC.
2019-12-22 | GSE128720 | GEO
Project description:Early-onset preeclampsia (EOPE) is a severe pregnancy complication associated with significant maternal and fetal morbidity and mortality. Currently, there is a critical need for accurate, non-invasive biomarkers to facilitate early diagnosis and effective management of EOPE. In this study, we aimed to investigate the transcriptional alterations and non-invasive biomarker potential of peripheral blood microRNAs in patients with EOPE. Through our research, we successfully identified two reliable plasma miRNA biomarkers and proposed a circulating two-miRNA panel for the non-invasive early detection of EOPE. Additionally, we independently validated our findings in different patient cohorts using various technological platforms.
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Project description:Autoimmune hepatitis (AIH) can be challenging to distinguish from other chronic liver diseases such as metabolic dysfunction-associated steatotic liver disease (MASLD). We applied advanced proteomic analysis to paired liver and plasma samples from newly diagnosed AIH patients, MASLD patients, and healthy controls to uncover disease-specific pathways and biomarkers. We quantified 7632 liver and 556 plasma proteins, identifying significant differences in 2521 liver and 227 plasma proteins between AIH and healthy individuals. A machine learning model based on plasma proteomics accurately distinguished AIH from MASLD and healthy controls (AUC = 0.91), with validation in the UK Biobank confirming diagnostic value for several candidate biomarkers. This study highlights distinct metabolic and immune signatures in AIH and supports the utility of plasma proteomics in non-invasive disease classification.
2025-07-17 | PXD065892 | Pride
Project description:Uric acid has garnered increasing attention for its association with metabolic dysfunction-associated steatotic liver disease (MASLD) in recent cross-sectional studies, although detailed understanding of its involvement remains limited. This study confirms a strong association between urate levels and elevated risk of both MASLD and type 2 diabetes (T2D) through a large-scale observational analysis of UK Biobank data. However, Mendelian randomization (MR) analysis involving over 2 million samples identified only causal effects of urate on serum triglyceride levels and the risk of T2D. Additionally, a targeted metabolomics study involving elderly Chinese participants revealed that, rather than UA, allantoin—a byproduct of UA oxidation—was significantly elevated in individuals with dyslipidemia or T2D. Notably, a significant negative correlation was found between serum allantoin level and fasting glucose, as well as serum triglyceride and cholesterol levels. Animal studies demonstrated that allantoin exacerbates hepatic lipid accumulation and glucose intolerance in mice fed a high-fat diet, which was accompanied by increased hepatic lipid biogenesis and reduced bile acid production. Interestingly, our findings indicate that allantoin exhibits a strong binding affinity for PPARα, suggesting that it may act as an inhibitor of PPARα, thereby promoting the progression of MASLD. These results underscore the critical role of allantoin, rather than UA, in the development of MASLD, offering valuable insights for the prediction and management of hepatic metabolic disorders.
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Project description:This study aimed to establish and characterize an in vitro model of human intestinal organoids isolated from duodenal samples of patients with non-fibrotic MASLD and those with MASLD-cirrhosis. Whole transcriptome analysis and the energetic and redox status of the organoids were assessed to characterize intestinal functional impairment in the context of MASLD. We used microarrays to detail the whole transcriptome dysregulation underlying intestinal dysfunction in organoids isolated from chirrotic versus non-fibrotic MASLD patients.
2025-09-04 | GSE299719 | GEO
Project description:A novel urinary microRNA biomarker panel for detecting gastric cancer
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Project description:Mutations of nuclear lamina-associated proteins LMNA and ZMPSTE24 have been associated with fatty liver. We report that the changes at the nuclear envelope we described in MASLD patients are caused by downregulation of ZMPSTE24, an enzyme that processes prelamin to mature lamin A. In addition, Zmpste24 mutant mice develop hepatic steatosis and exhibit upregulation of p53 target genes. p53 activity is also induced in genes differentially expressed in MASLD patients. Furthermore, p53 regulates genes bound by FOXA2 in these individuals, corresponding to observations in Zmpste24 mutants. In contrast, expression of glucose and insulin regulated genes is reduced in MASLD patients, suggesting altered glucose metabolism and insulin resistance, hallmarks of type 2 diabetes (T2D). Hence, our genomics data show that MASLD patients with severe steatosis but yet without MASH are already suffering from severe metabolic consequences and underscore the need for treatment at this stage of the disease.
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Project description:Allantoin promotes MASLD progression
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