ArticleHepatology (Baltimore, Md.)2020
Sestrin 3 Protects Against Diet-Induced Nonalcoholic Steatohepatitis in Mice Through Suppression of Transforming Growth Factor β Signal Transduction.
Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Effect of bicyclol on blood biomarkers of NAFLD: a systematic review and meta-analysis.BMJ open · 2020Pooled it
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- Effects of Chronic Moderate Alcohol Intake on Metabolic Phenotypes and Gut Microbiota in Lean and Obese Mice with Distinct Dietary Structures.Nutrients · 2025Article
- SESN3 restrains the progress of idiopathic pulmonary fibrosis by targeting the activity of FOSL2.Biology direct · 2025Article
- Restoration of Sestrin 3 Expression Mitigates Cardiac Oxidative Damage in Ischemia-Reperfusion Injury Model.Antioxidants (Basel, Switzerland) · 2025Article
- Role of sestrins in metabolic and aging-related diseases.Biogerontology · 2024Review
- ATG14 plays a critical role in hepatic lipid droplet homeostasis.Metabolism: clinical and experimental · 2023Article
- Article
- Enhanced Expression of ARK5 in Hepatic Stellate Cell and Hepatocyte Synergistically Promote Liver Fibrosis.International journal of molecular sciences · 2022Article
- Sirtuin 6 protects against hepatic fibrogenesis by suppressing the YAP and TAZ function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- The potential of mecciRNA in hepatic stellate cell to regulate progression of nonalcoholic hepatitis.Journal of translational medicine · 2022Article
- Smad3 Phospho-Isoform Signaling in Nonalcoholic Steatohepatitis.International journal of molecular sciences · 2022Review
- The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022Review
- Combined Use of Bicyclol and Berberine Alleviates Mouse Nonalcoholic Fatty Liver Disease.Frontiers in pharmacology · 2022Article
- Nootkatone, a Sesquiterpene Ketone FromFrontiers in pharmacology · 2022Article
- SIRT6 controls hepatic lipogenesis by suppressing LXR, ChREBP, and SREBP1.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- Oncogenic role of early growth response-1 in liver cancer through the regulation of the microRNA-675/sestrin 3 and the Wnt/β-catenin signaling pathway.Bioengineered · 2021Article
- Article
- Signal Transduction and Molecular Regulation in Fatty Liver Disease.Antioxidants & redox signaling · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Sestrin 3 (Sesn3) belongs to the three-member sestrin protein family. Sestrins have been implicated in antioxidative stress, adenosine monophosphate-activated protein kinase and mammalian target of rapamycin signal transduction, and metabolic homeostasis. However, the role of Sesn3 in the development of nonalcoholic steatohepatitis (NASH) has not been previously studied. In this work, we generated Sesn3 whole-body knockout and liver-specific transgenic mice to investigate the hepatic function of Sesn3 in diet-induced NASH. With only 4 weeks of dietary treatment, Sesn3 knockout mice developed severe NASH phenotype as characterized by hepatic steatosis, inflammation, and fibrosis. Strikingly, after 8-week feeding with a NASH-inducing diet, Sesn3 transgenic mice were largely protected against NASH development. Transcriptomic analysis revealed that multiple extracellular matrix-related processes were up-regulated, including transforming growth factor β (TGF-β) signaling and collagen production. Further biochemical and cell biological analyses have illustrated a critical control of the TGF-β-mothers against decapentaplegic homolog (Smad) pathway by Sesn3 at the TGF-β receptor and Smad3 levels. First, Sesn3 inhibits the TGF-β receptor through an interaction with Smad7; second, Sesn3 directly inhibits the Smad3 function through protein-protein interaction and cytosolic retention. Conclusion: Sesn3 is a critical regulator of the extracellular matrix and hepatic fibrosis by suppression of TGF-β-Smad3 signaling.
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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.