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Aldehydes alter TGF-β signaling and induce obesity and cancer

GSE273561 Homo sapiens; Mus musculus Expression profiling by high throughput sequencing 27 samples Submitted 2024/08/06 Platform GPL24676Platform GPL24247
Summary
Obesity and fatty liver diseases-metabolic dysfunction-associated steatotic liver disease (MASLD and MASH) affect over a third of the global population and are exacerbated in individuals with reduced functional aldehyde dehydrogenase 2 (ALDH2), observed in approximately 560 million people. Current treatment to prevent disease progression to cancer remains inadequate, requiring innovative approaches. We observe that Aldh2-/- and Aldh2-/-Sptbn1+/- (ASKO) mice develop phenotypes of human Metabolic Syndrome (MetS) and MASH with altered lipid metabolism and TGF-β signaling, leading to pro-fibrotic and pro-oncogenic phenotypes, which is restored to normal with siRNA to SPTBN1. Significantly, therapeutic inhibition of SPTBN1 blocks MASH and fibrosis in a human 3D MASH model. This study identifies SPTBN1 as a critical regulator of the functional phenotype of toxic aldehyde-induced MASH and a potential therapeutic target.
Published in
Aldehydes alter TGF-β signaling and induce obesity and cancer
Yang X, Bhowmick K, Rao S et al. · Cell reports 2024 · PMID 39217614 · doi:10.1016/j.celrep.2024.114676
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Direct links to NCBI, no account and no request form: the whole study as GSE273561_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 27 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1142410 and SRA study SRP523313. Searching any of these in the dataset finder brings you back here.

Study design
27 conditions, each sampled once — no replicated groups

Read from 27 sample titles: 27 distinct titles with little repetition. Check it against the sample list below before relying on it.

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