ReviewAlimentary pharmacology & therapeutics2023
Review article: the role of HSD17B13 on global epidemiology, natural history, pathogenesis and treatment of NAFLD.
Review in Alimentary pharmacology & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
38 citing papers in PubMed, 49 citations in OpenAlex.
- Metabolic Dysfunction-Associated Steatotic Disease and Genetic Risk in Germany-An Observational Real-World Cohort Study.United European gastroenterology journal · 2026Observational
- Prime editing models the MTARC1 A165T variant in human liver organoids, demonstrating reduced steatosis, inflammation, and fibrosis.Hepatology communications · 2026Article
- Steatotic liver disease in Latin America: current views and perspectives.Nature reviews. Gastroenterology & hepatology · 2026Review
- Genetic testing in liver diseases: Clinical applications.JHEP reports : innovation in hepatology · 2026Review
- Risk assessment in metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction and alcohol-related liver disease: current approaches and future directions.Clinical and molecular hepatology · 2026Review
- Article
- CIDEB and CGI-58 differentially regulate liver lipid-droplet cholesterol to modulate metabolic dysfunction-associated steatohepatitis severity.Cell reports · 2026Article
- Unveiling novel macrophage-specific biomarkers in MASH through single-cell sequencing for diagnostic modeling.Journal of lipid research · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Genetic Predisposition to MASLD: Potential for Therapeutic Management.International journal of molecular sciences · 2026Review
- Targeting Undruggable Proteins: The siRNA Revolution Beyond Small Molecules - Advances, Challenges, and Future Prospects in Therapeutic Innovation.Current gene therapy · 2026Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease and Emerging Oligonucleotide Therapies.International journal of biological sciences · 2026Review
- Current status of research on the risk factors and pathogenesis of metabolic dysfunction-associated steatotic liver disease.Frontiers in endocrinology · 2026Review
- Phenotypic Screening Coupled with AI-Driven Target Deconvolution Identifies α-Terthienyl as a Dual DPP-IV/HSD17β13 Modulator with Efficacy in a Mouse Model of MASLD.bioRxiv : the preprint server for biology · 2025Article
- Genetic predeterminants and recent advancements in steatotic liver disease: A roadmap toward precision hepatology.World journal of hepatology · 2025Review
- Integrated bioinformatics decoding of the MASLD ceRNA network reveals novel therapeutic targets.Clinical and experimental medicine · 2025Article
- Crosstalk Between Metabolic Dysfunction-Associated Steatotic Liver Disease and Atrial Fibrillation: Shared Mechanism, Diagnostic Integration, and Management Implications.Life (Basel, Switzerland) · 2025Review
- Genetic polymorphisms associated with metabolic dysfunction-associated steatotic liver disease and cardiometabolic risk susceptibility in the Chinese Han population.Human genomics · 2025Article
- Beyond obesity: lean metabolic dysfunction-associated steatohepatitis from unveiling molecular pathogenesis to therapeutic advancement.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hydroxysteroid 17β-dehydrogenase 13 (Hsd17b13) knockdown attenuates liver steatosis in high-fat diet obese mice.Experimental physiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) occurs in around a quarter of the global population and is one of the leading causes of chronic liver disease. The phenotypic manifestation and the severity of NAFLD are influenced by an interplay of environmental and genetic factors. Recently, several inactivating variants in the novel 17-Beta hydroxysteroid dehydrogenase 13 (HSD17B13) gene have been found to be associated with a reduced risk of chronic liver diseases, including NAFLD.
aimsTo review the existing literature on the epidemiology of HSD17B13 and discuss its role in the natural history, disease pathogenesis and treatment of NAFLD.
methodsWe extensively searched relevant literature in PubMed, Google Scholar, clinicaltrials.gov and the reference list of articles included in the review.
resultsHSD17B13 is a liver-specific, lipid droplet (LD)-associated protein that has enzymatic pathways involving steroids, pro-inflammatory lipid mediators and retinol. The estimated prevalence of the best characterised HSD17B13 variant (rs72613567) ranges from 5% in Africa to 34% in East Asia. Loss-of-function variants in HSD17B13 are protective against the progression of NAFLD from simple steatosis to non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis and hepatocellular carcinoma. Emerging data from mechanistic and preclinical studies with RNA interference (RNAi) and small molecule agents indicate that inhibiting HSD17B13 activity may prevent NAFLD progression.
conclusionsThe loss-of-function polymorphisms of the newly identified HSD17B13 gene mitigate the progression of NAFLD. It is important to understand the exact mechanism by which these variants exert a protective effect and implement the gathered knowledge in the treatment of NAFLD.
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What OpenQuestion holds
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 OpenQuestion graph.