ArticleJournal of molecular cell biology2024
HSD17B13 liquid-liquid phase separation promotes leukocyte adhesion in chronic liver inflammation.
Article in Journal of molecular cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Autophagy in the liver.Autophagy reports · 2026Review
- Molecular mechanisms mediated by liquid-liquid phase separation in chronic liver disease progression.iScience · 2025Review
- Unveiling the dynamic drivers: phase separation's pivotal role in stem cell biology and therapeutic potential.Stem cell research & therapy · 2025Review
- Lipidomic Profiling Reveals HSD17B13 Deficiency-Associated Dysregulated Hepatic Phospholipid Metabolism in Aged Mice.Metabolites · 2025Article
- Role of genetic variants and DNA methylation of lipid metabolism-related genes in metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The rs72613567:TA polymorphism in 17-beta hydroxysteroid dehydrogenase 13 (HSD17B13) has been found to reduce the progression from steatosis to metabolic dysfunction-associated steatohepatitis (MASH). In this study, we sought to define the pathogenic role of HSD17B13 in triggering liver inflammation. Here, we demonstrate that HSD17B13 forms liquid-liquid phase separation (LLPS) around lipid droplets in the livers of MASH patients. The dimerization of HSD17B13 supports the LLPS formation and promotes its enzymatic function. HSD17B13 LLPS increases the biosynthesis of platelet activating factor (PAF), which in turn promotes fibrinogen synthesis and leukocyte adhesion. Blockade of the PAF receptor or STAT3 pathway inhibits the fibrinogen synthesis and leukocyte adhesion. Importantly, adeno-associated viral-mediated xeno-expression of human HSD17B13 exacerbates western diet/carbon tetrachloride-induced liver inflammation in Hsd17b13-/- mice. In conclusion, our results suggest that HSD17B13 LLPS triggers liver inflammation by promoting PAF-mediated leukocyte adhesion, and targeting HSD17B13 phase transition could be a promising therapeutic approach for treating hepatic inflammation in chronic liver disease.
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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.