ArticleJournal of hepatology2022
ADAMTSL2 protein and a soluble biomarker signature identify at-risk non-alcoholic steatohepatitis and fibrosis in adults with NAFLD.
Article in Journal of hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Conserved hepatic RNA signatures across multiple cohorts reveal novel mechanistic clues for advanced fibrosis in human MASLD.Hepatology communications · 2026Pooled it
- KASL clinical practice guidelines for noninvasive tests to assess liver fibrosis in chronic liver disease.Clinical and molecular hepatology · 2024Guideline
- SomaLogic proteomics reveals new biomarkers and provides mechanistic, clinical insights into Acetyl coA Carboxylase (ACC) inhibition in Non-alcoholic Steatohepatitis (NASH).Scientific reports · 2024Trial
- Omics-based Decoding of Metabolic Dysfunction-associated Fatty Liver Disease: From Pathogenesis to Clinical Translation.Journal of clinical and translational hepatology · 2026Review
- Gene-Based Clustering Identifies QSOX1 and IL1RAP as Biomarkers of Metabolic Dysfunction-Associated Steatotic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Review
- Life's crucial 9, plasma proteomics, and the risk of major complications and mortality in MASLD.npj metabolic health and disease · 2026Article
- Proteomic Signatures of 3-Year Progression From Impaired Fasting Glucose to Diabetes: The Atherosclerosis Risk in Communities (ARIC) Study.Diabetes care · 2026Article
- Integrated GWAS and eQTL Colocalization Identified Candidate Genes for Growth Traits in Pigs.Biology · 2026Article
- The Pathogenic ADAMTSL2 D167N Variant Causes Geleophysic Dysplasia-Like Connective Tissue Changes in Mice.The American journal of pathology · 2026Article
- ADAMTS4 elicits myeloid-derived immune cell recruitment and liver fibrogenesis in metabolic dysfunction-associated steatotic liver disease.Signal transduction and targeted therapy · 2026Article
- Article
- Serum Proteomics of Insulin Resistance Disorders Distinguish MASLD From Lipodystrophy and Insulin Receptor Defects.The Journal of clinical endocrinology and metabolism · 2026Article
- Plasma IGFBP7 improves risk reclassification for liver-related outcomes: Insights from proteo-transcriptomic profiling.JHEP reports : innovation in hepatology · 2026Article
- A high FIB-4 score may be an early sign of severe liver involvement in patients with primary antibody deficiencies.Turkish journal of medical sciences · 2026Article
- Transcriptomic and Proteomic Analyses Identify THBS2, VWF, NFASC, and AKR1B10 as Diagnostic Biomarkers for Advanced Fibrosis in NAFLD.Journal of inflammation research · 2026Article
- Panomics in metabolic dysfunction-associated steatotic liver disease: unravelling the drivers of disease heterogeneity.Clinical and molecular hepatology · 2026Review
- Circulating causal protein networks linked to future risk of myocardial infarction.Nature communications · 2025Article
- Low-Abundance Proteomics Reveal Pleiotrophin and Fibroblast Growth Factor-21 as Biomarkers of Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2025Article
- Modulation of metabolic, inflammatory and fibrotic pathways by semaglutide in metabolic dysfunction-associated steatohepatitis.Nature medicine · 2025Article
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19 authors.
Funding
Abstract
BACKGROUND &
aimsIdentifying fibrosis in non-alcoholic fatty liver disease (NAFLD) is essential to predict liver-related outcomes and guide treatment decisions. A protein-based signature of fibrosis could serve as a valuable, non-invasive diagnostic tool. This study sought to identify circulating proteins associated with fibrosis in NAFLD.
methodsWe used aptamer-based proteomics to measure 4,783 proteins in 2 cohorts (Cohort A and B). Targeted, quantitative assays coupling aptamer-based protein pull down and mass spectrometry (SPMS) validated the profiling results in a bariatric and NAFLD cohort (Cohort C and D, respectively). Generalized linear modeling-logistic regression assessed the ability of candidate proteins to classify fibrosis.
resultsFrom the multiplex profiling, 16 proteins differed significantly by fibrosis in cohorts A (n = 62) and B (n = 98). Quantitative and robust SPMS assays were developed for 8 proteins and validated in Cohorts C (n = 71) and D (n = 84). The A disintegrin and metalloproteinase with thrombospondin motifs like 2 (ADAMTSL2) protein accurately distinguished non-alcoholic fatty liver (NAFL)/non-alcoholic steatohepatitis (NASH) with fibrosis stage 0-1 (F0-1) from at-risk NASH with fibrosis stage 2-4, with AUROCs of 0.83 and 0.86 in Cohorts C and D, respectively, and from NASH with significant fibrosis (F2-3), with AUROCs of 0.80 and 0.83 in Cohorts C and D, respectively. An 8-protein panel distinguished NAFL/NASH F0-1 from at-risk NASH (AUROCs 0.90 and 0.87 in Cohort C and D, respectively) and NASH F2-3 (AUROCs 0.89 and 0.83 in Cohorts C and D, respectively). The 8-protein panel and ADAMTSL2 protein had superior performance to the NAFLD fibrosis score and fibrosis-4 score.
conclusionThe ADAMTSL2 protein and an 8-protein soluble biomarker panel are highly associated with at-risk NASH and significant fibrosis; they exhibited superior diagnostic performance compared to standard of care fibrosis scores. LAY SUMMARY: Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of liver disease worldwide. Diagnosing NAFLD and identifying fibrosis (scarring of the liver) currently requires a liver biopsy. Our study identified novel proteins found in the blood which may identify fibrosis without the need for a liver biopsy.
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