ArticleCell biochemistry and biophysics2025
C6orf120 Deficiency Inhibits Hepatic Stellate Cell Activation by Upregulating RARβ Signaling.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- C6ORF120 regulates hepatic lipid metabolism through PPAR signaling pathway in metabolic dysfunction-associated steatotic liver disease.Functional & integrative genomics · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
Vitamin A (VA) and its active form, retinoic acid (RA), are crucial for preserving hepatic stellate cells (HSCs) quiescence and reversing fibrosis. While C6orf120 is known to be involved in HSC activation, its role in RA signaling is unclear. This study found that C6orf120 knockdown markedly reduced CCL4-induced liver fibrosis and TGF-β1-induced activation in LX-2 cells, a human HSC line. This inhibition was associated with enhanced RA signaling, particularly affecting the RA receptor beta (RARβ). Inhibition of RARβ significantly reversed the protective effects of C6orf120 knockdown, indicating that RARβ signaling contributes to the inhibitory effect of C6orf120 knockdown on HSC activation. Our results reveal that C6orf120 inhibition could be a therapeutic strategy for liver fibrosis by regulating RARβ signaling.
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Registered trials
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