ArticleCell communication and signaling : CCS2026
Identification of the E3 ligase TRIM21 as a crucial regulator of STAT1 in metabolic dysfunction-associated steatohepatitis.
Article in Cell communication and signaling : CCS, 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
10 authors.
Funding
Abstract
BACKGROUND AND
aimsMetabolic associated fatty liver disease (MAFLD) is closely associated with metabolic disorders, including central obesity, dyslipidaemia, hypertension, hyperglycaemia and persistent abnormalities of liver function tests. Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive form of MAFLD, characterized by chronic inflammation and accumulation of fat in liver tissue. Currently, no pharmacological interventions specifically tailored for MASH are approved. Signal transducer and activator of transcription 1 (STAT1) is the key transcription factor of the JAK-STAT signaling pathway, participating in physiological and pathological processes such as immune regulation, inflammatory response, antiviral defense, cell proliferation and apoptosis, and plays an important regulatory role in the occurrence and development of MASH. However, the post-translational modification of STAT1 in MASH is unclarified. METHODS AND
resultsWe identified that STAT1 was increased in MASH due to the inhibition of ubiquitination levels. Mechanistically, we showed that TRIM21 directly binds to STAT1 and promotes STAT1 degradation by accelerating lysine residue at 48 site-linked ubiquitination. Through gain- and loss-of-function studies in Trim21 knockout mice and adenovirus-treated models (in vivo and in vitro), we further demonstrated TRIM21's protective role in MASH. Collectively, our investigations have revealed that TRIM21 suppresses hepatocyte steatosis relying on regulating STAT1.
conclusionThe ubiquitination of STAT1 in MASH is regulated by TRIM21 which is a key suppressor of MASH. TRIM21 acts as a negative regulator in hepatic steatosis and offers potential therapeutic opportunities for MASH.
Indexed as
Identifiers
What Socratic 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 Socratic graph.