ArticleInternational journal of biological sciences2026
Histone acetyltransferases and deacetylase 6 (HDAC6) Promotes Hepatic Stellate Cell Activation and Liver Fibrosis.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis results from excessive extracellular matrix (ECM) deposition following chronic hepatocyte injury. Hepatic stellate cell (HSC) activation is central to fibrogenesis; however, the regulatory mechanisms controlling this process remain unclear. Protein acetylation, regulated by histone acetyltransferases and deacetylases (HDACs), modulates gene expression and protein stability. To date, no studies have explored acetylation dynamics during HSC activation using proteomic approaches. In this study, we investigated the role of acetylation in HSC activation and liver fibrosis. Proteomic profiling of primary mouse HSCs was performed to assess global protein acetylation and the expression of HDACs and SIRTs during HSC activation. Activated HSCs exhibited reduced global protein acetylation, increased HDAC2/3/6 expression, and decreased SIRTs expression. Selective inhibition of HDAC6, but not HDAC2/3, suppressed TGF-β-induced HSC activation. TGF-β increased HDAC6 expression via Smad3-dependent transcription, and HDAC6 promoted fibrogenic gene expression through Smad activation. Proteomic screening identified acetyl-CoA acetyltransferase 1 (ACAT1) as a novel HDAC6 substrate; HDAC6 overexpression enhanced ACAT1 binding and reduced its acetylation.
Indexed as
Identifiers
What OpenQuestion holds
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.