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Transcription factor REST regulates activation and growth of human Hepatic Stellate Cells

GSE289433 Homo sapiens Expression profiling by high throughput sequencing 8 samples Submitted 2026/01/30 Platform GPL24676
Summary
Activation of hepatic stellate cells (HSC) is a key component in the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) to metabolic-associated steatohepatitis (MASH) and hepatocellular carcinoma (HCC). Targeting HSC activation to prevent MASH and HCC pathogenesis showed promise in mouse models, suggesting that development of therapeutic strategies to abrogate HSC activation could be a promising approach to combat liver disease. Metabolic alterations were suggested to play a pivotal role in HSC activation, yet the mechanisms linking these processes have not been fully elucidated. Here we observe a key role of the RE1-silencing transcription factor (REST) in linking HSC activation, lipid utilization, and mitochondrial metabolism, suggesting that REST is a mechanistic link between HSC metabolism and activation.
Published in
Proliferation of activated hepatic stellate cells requires REST
Shavva VS, Tarnawski L, Dai W et al. · Molecular medicine (Cambridge, Mass.) 2026 · PMID 41606712 · doi:10.1186/s10020-025-01406-z
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Also filed as BioProject PRJNA1222899 and SRA study SRP563494. Searching any of these in the dataset finder brings you back here.

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