ArticleThe Journal of clinical investigation2024
TRIM56 protects against nonalcoholic fatty liver disease by promoting the degradation of fatty acid synthase.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 53 citations in OpenAlex.
- Ovarian tumor domain-containing protein 1 deficiency attenuates metabolic dysfunction-associated steatotic liver disease by promoting the ubiquitination of HSP90α in hepatocytes.Molecular biomedicine · 2026Article
- Kaempferol Ameliorates Non-Alcoholic Fatty Liver Disease by Targeting TRIM56 to Regulate Lipid Metabolism.International journal of molecular sciences · 2026Article
- MIF-mediated crosstalk between THRSP + hepatocytes and CD74 + lipid-associated macrophages in hepatic periportal zone drives MASH.Hepatology (Baltimore, Md.) · 2026Article
- A Multi-Omics Integration Analysis Reveals ThatAntioxidants (Basel, Switzerland) · 2026Article
- Ufmylation-Deficient DDRGK1 Ameliorates Obesity by Inhibiting FASN-Mediated Adipocyte Lipogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SiRNA-based inactivation of Angptl3 alleviates high-fat diet-induced MAFLD and atherosclerosis in LDLR-deficient hamsters.Lipids in health and disease · 2026Article
- PKC-iota drives EGFR-TKI resistance in EGFR-mutated NSCLC by phosphorylating FASN to reprogram lipid metabolism.Translational lung cancer research · 2026Article
- Protein lactylation in metabolic dysfunction-associated steatotic liver disease: a mechanistic review.Diabetology & metabolic syndrome · 2026Review
- TRIM56 Aggravates Cerebral Ischemia-Reperfusion Injury via Inhibiting KLF4-Activated Ferroptosis Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- [EVA1A overexpression improves non-alcoholic fatty liver disease in mice by regulating lipid metabolism and promoting lipophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- The implications of FASN in viral infection and related diseases: a promising target in antiviral therapies.Frontiers in cellular and infection microbiology · 2026Review
- Drug Repurposing for Metabolic-Associated Fatty Liver Disease: Current Evidence, Challenges, and Future Perspectives.Drug design, development and therapy · 2026Review
- Identification of key genes potentially associated with bladder cancer development by common plasticizers: an integrated transcriptomics and network toxicology study.Frontiers in oncology · 2026Article
- Obesity-Associated TRIM15 Promotes the Proliferation of Esophageal Adenocarcinoma Through the YY2/FOXRED1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Disrupted Lipid Metabolism Aggravates Ischemic Brain Injury: Targeting FDFT1 for Stroke Therapy.Molecular neurobiology · 2025Article
- Protein palmitoylation in hepatic diseases: Functional insights and therapeutic strategies.Journal of advanced research · 2025Review
- Revisiting the role of GDF15 in atherosclerosis in mouse and human.Acta pharmacologica Sinica · 2025Article
- Deficiency of Ugcg in LSECs alleviates high-fat diet-induced MASLD.Hepatology communications · 2025Article
- Ubiquitination and ubiquitin-like modifications in metabolic dysfunction-associated steatotic liver disease: mechanisms and implications.BMB reports · 2025Review
- Post-translational modifications in the pathophysiological process of metabolic dysfunction‑associated steatotic liver disease.Cell & bioscience · 2025Review
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Authors and funding
24 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses a disease continuum from simple steatosis to nonalcoholic steatohepatitis (NASH). However, there are currently no approved pharmacotherapies for NAFLD, although several drugs are in advanced stages of clinical development. Because of the complex pathophysiology and heterogeneity of NAFLD, the identification of potential therapeutic targets is clinically important. Here, we demonstrated that tripartite motif 56 (TRIM56) protein abundance was markedly downregulated in the livers of individuals with NAFLD and of mice fed a high-fat diet. Hepatocyte-specific ablation of TRIM56 exacerbated the progression of NAFLD, while hepatic TRIM56 overexpression suppressed it. Integrative analyses of interactome and transcriptome profiling revealed a pivotal role of TRIM56 in lipid metabolism and identified the lipogenesis factor fatty acid synthase (FASN) as a direct binding partner of TRIM56. TRIM56 directly interacted with FASN and triggered its K48-linked ubiquitination-dependent degradation. Finally, using artificial intelligence-based virtual screening, we discovered an orally bioavailable small-molecule inhibitor of FASN (named FASstatin) that potentiates TRIM56-mediated FASN ubiquitination. Therapeutic administration of FASstatin improved NAFLD and NASH pathologies in mice with an optimal safety, tolerability, and pharmacokinetics profile. Our findings provide proof of concept that targeting the TRIM56/FASN axis in hepatocytes may offer potential therapeutic avenues to treat NAFLD.
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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.