ReviewActa pharmaceutica Sinica. B2025
The ubiquitin-proteasome system: A potential target for the MASLD.
Review in Acta pharmaceutica Sinica. B, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis.Nature metabolism · 2026Article
- Identification of Proteomic Markers for Monitoring Direct Toxic Liver Injury (DTLI): Profiling Hepatoprotective Effects of Plant Polyphenols.International journal of molecular sciences · 2026Article
- Deubiquitinating Enzymes as Therapeutic Candidates in Hepatocellular Carcinoma and Other Liver Disease.International journal of molecular sciences · 2026Review
- Cuproptosis: potential new direction in liver-related diseases research and treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Nuciferine inhibits pressure overload-induced cardiac remodeling by activating the SENP1-ACSL4-ferroptosis axis.Journal of advanced research · 2026Article
- Blocking TRIM47-mediated HNF4Acta pharmaceutica Sinica. B · 2026Article
- Ubiquitination modifications as central regulators of metabolic dysfunction in type 2 diabetes mellitus.Frontiers in endocrinology · 2026Review
- FBXL8 Stabilizes IκBα and Negatively Regulated NF-κB Activation to Suppress Pancreatic Cancer Progression.International journal of biological sciences · 2026Article
- Evaluation of the CHG index for identifying metabolic dysfunction associated steatotic liver disease: evidence from two independent Asian non-obese populations.Frontiers in nutrition · 2026Article
- Liver-targeted degradation of BRD4 reverses hepatic fibrosis and enhances metabolism in murine models.Theranostics · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD), the most prevalent chronic liver condition globally, lacks adequate and effective therapeutic remedies in clinical practice. Recent studies have increasingly highlighted the close connection between the ubiquitin-proteasome system (UPS) and the progression of MASLD. This relationship is crucial for understanding the disease's underlying mechanism. As a sophisticated process, the UPS govern protein stability and function, maintaining protein homeostasis, thus influencing a multitude of elements and biological events of eukaryotic cells. It comprises four enzyme families, namely, ubiquitin-activating enzymes (E1), ubiquitin-conjugating enzymes (E2), ubiquitin-protein ligases (E3), and deubiquitinating enzymes (DUBs). This review aims to delve into the array of pathways and therapeutic targets implicated in the ubiquitination within the pathogenesis of MASLD. Therefore, this review unveils the role of ubiquitination in MASLD while spotlighting potential therapeutic targets within the context of this disease.
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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.