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Hepatocyte-derived Pumilio1-enriched exosomes inhibit HSC activation by suppressing tropomyosin-4 translation

GSE295362 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2025/04/27 Platform GPL16791
Summary
Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the most common chronic liver disease globally. Abnormal crosstalk between hepatocytes and hepatic stellate cells (HSCs) leads to liver fibrosis and aggravates MASLD. We explored the role of the RNA-binding protein Pumilio in this process.
Published in
Hepatocyte-derived Pumilio1-enriched exosomes inhibit HSC activation by suppressing tropomyosin-4 translation
Wan Z, Cai X, Liu X et al. · Hepatology communications 2025 · PMID 40689527 · doi:10.1097/HC9.0000000000000759
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Also filed as BioProject PRJNA1254274 and SRA study SRP580572. Searching any of these in the dataset finder brings you back here.

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