ReviewFrontiers in molecular biosciences2021
HSD17B13: A Potential Therapeutic Target for NAFLD.
Review in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 52 citations in OpenAlex.
- Advancing risk gene discovery across the allele frequency spectrum.HGG advances · 2026Review
- Paediatric metabolic dysfunction-associated steatotic liver disease (MASLD): a growing health concern in the age of childhood obesity.BMJ paediatrics open · 2026Review
- Disease-driven loss of inactive HSD17B13 isoforms enhances enzymatic output in MASH and counters protective rs72613567:TA variant.JHEP reports : innovation in hepatology · 2026Article
- GCKR genetic variants and circulating FGF21 identify a metabolic risk signature in metabolic dysfunction-associated steatotic liver disease.BMC gastroenterology · 2026Article
- Genetic modulators of metabolic dysfunction-associated steatotic liver disease (MASLD) and their epistatic interactions: from in vitro and animal models to clinical outcomes.BMC medical genomics · 2026Review
- Pharmacogenomic Pathways Underlying Variable Vedolizumab Response in Crohn's Disease Patients: A Rare-Variant Analysis.Biomedicines · 2026Article
- Article
- Metabolic Dysfunction-Associated Steatotic Liver Disease and Emerging Oligonucleotide Therapies.International journal of biological sciences · 2026Review
- Mitochondrial dysfunction and lipid droplet dynamics in MASH: HSD17B13 as a therapeutic target.Frontiers in cell and developmental biology · 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
- Article
- C6ORF120 regulates hepatic lipid metabolism through PPAR signaling pathway in metabolic dysfunction-associated steatotic liver disease.Functional & integrative genomics · 2025Article
- Hydroxysteroid 17β-dehydrogenase 13 (Hsd17b13) knockdown attenuates liver steatosis in high-fat diet obese mice.Experimental physiology · 2025Article
- Antifibrotic therapies for metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2025Review
- Characterizing primary and secondary senescence in vivo.Nature aging · 2025Article
- Gene-based therapies for steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Lipidomic Profiling Reveals HSD17B13 Deficiency-Associated Dysregulated Hepatic Phospholipid Metabolism in Aged Mice.Metabolites · 2025Article
- Development, opportunities, and challenges of siRNA nucleic acid drugs.Molecular therapy. Nucleic acids · 2025Review
- Unraveling Metabolic Dysfunction-Associated Steatotic Liver Disease Through the Use of Omics Technologies.International journal of molecular sciences · 2025Review
- Therapeutic Targets and Approaches to Manage Inflammation of NAFLD.Biomedicines · 2025Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD), especially in its inflammatory form (steatohepatitis, NASH), is closely related to the pathogenesis of chronic liver disease. Despite substantial advances in the management of NAFLD/NASH in recent years, there are currently no efficacious therapies for its treatment. The biogenesis and expansion of lipid droplets (LDs) are critical pathophysiological processes in the development of NAFLD/NASH. In the past decade, increasing evidence has demonstrated that lipid droplet-associated proteins may represent potential therapeutic targets for the treatment of NAFLD/NASH given the critical role they play in regulating the biogenesis and metabolism of lipid droplets. Recently, HSD17B13, a newly identified liver-enriched, hepatocyte-specific, lipid droplet-associated protein, has been reported to be strongly associated with the development and progression of NAFLD/NASH in both mice and humans. Notably, human genetic studies have repeatedly reported a robust association of HSD17B13 single nucleotide polymorphisms (SNPs) with the occurrence and severity of NAFLD/NASH and other chronic liver diseases (CLDs). Here we briefly overview the discovery, tissue distribution, and subcellular localization of HSD17B13 and highlight its important role in promoting the pathogenesis of NAFLD/NASH in both experimental animal models and patients. We also discuss the potential of HSD17B13 as a promising target for the development of novel therapeutic agents for NAFLD/NASH.
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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.