ArticleThe American journal of pathology2002
STAT-3 overexpression and p21 up-regulation accompany impaired regeneration of fatty livers.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 96 citations in OpenAlex.
- Loss ofJHEP reports : innovation in hepatology · 2025Article
- High fat diet-induced downregulation of TRPV2 mediates hepatic steatosis via p21 signalling.Journal of physiology and biochemistry · 2024Article
- Opportunities and challenges: interleukin-22 comprehensively regulates polycystic ovary syndrome from metabolic and immune aspects.Journal of ovarian research · 2023Review
- Adipose tissue induces a better liver regeneration after living liver donation in normal weight donors.Hepatobiliary surgery and nutrition · 2023Article
- Granulocyte colony-stimulating factor attenuates liver damage by M2 macrophage polarization and hepatocyte proliferation in alcoholic hepatitis in mice.Hepatology communications · 2022Article
- APAP-Induced IκBβ/NFκB Signaling Drives Hepatic Il6 Expression and Associated Sinusoidal Dilation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Single nucleotide polymorphisms in interleukin-6 attenuates hepatocytes injury in hypoxia/re-oxygenation via STAT3 signal pathway mediated autophagy.Molecular biology reports · 2021Article
- Liver Regeneration after Hepatectomy and Partial Liver Transplantation.International journal of molecular sciences · 2020Review
- Ischemia/Reperfusion Injury Revisited: An Overview of the Latest Pharmacological Strategies.International journal of molecular sciences · 2019Review
- Liver Regeneration after Acetaminophen Hepatotoxicity: Mechanisms and Therapeutic Opportunities.The American journal of pathology · 2019Review
- Resveratrol Improves Recovery and Survival of Diet-Induced Obese Mice Undergoing Extended Major (80%) Hepatectomy.Digestive diseases and sciences · 2019Article
- Inflammatory Cytokine TNFα Promotes the Long-Term Expansion of Primary Hepatocytes in 3D Culture.Cell · 2018Article
- Foie gras and liver regeneration: a fat dilemma.Cell stress · 2018Review
- Article
- Evaluation of safety for hepatectomy in a novel mouse model with nonalcoholic-steatohepatitis.World journal of gastroenterology · 2018Article
- Diabetes Mellitus and Liver Surgery: The Effect of Diabetes on Oxidative Stress and Inflammation.Mediators of inflammation · 2018Review
- Systems Analysis of the Complement-Induced Priming Phase of Liver Regeneration.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- STAT3 modulates β-cell cycling in injured mouse pancreas and protects against DNA damage.Cell death & disease · 2016Article
- Significant lethality following liver resection in A20 heterozygous knockout mice uncovers a key role for A20 in liver regeneration.Cell death and differentiation · 2015Article
- p62/SQSTM1 plays a protective role in oxidative injury of steatotic liver in a mouse hepatectomy model.Antioxidants & redox signaling · 2014Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Fatty liver is an important cause of morbidity in humans and is linked to impaired liver regeneration after liver injury, but the mechanisms for impaired liver regeneration remain unknown. In the normal liver, the interleukin (IL)-6/STAT-3 pathway is thought to play a central role in regeneration because this pathway is disrupted in IL-6-deficient mice that exhibit impaired liver regeneration after 70% partial hepatectomy (PH). To determine whether inhibition of STAT-3 is involved in fatty liver-related mitoinhibition, regenerative induction of STAT-3 was compared in normal mice and leptin-deficient ob/ob mice that have fatty livers and markedly impaired liver regeneration after PH. In both groups, two waves of STAT-3 activation were observed, the first in endothelia and the second in hepatocytes. Before PH, a significantly higher percentage of ob/ob endothelial and hepatocyte nuclei expressed phosphorylated (activated) STAT-3. After PH, phospho-STAT-3 accumulated in liver nuclei of lean mice and this response was markedly exaggerated in ob/ob mice. Moreover, a striking inverse correlation was noted between hepatocyte nuclear accumulation of phospho-STAT-3 and DNA synthesis (as assessed by bromodeoxyuridine labeling), as well as cyclin D1 mRNA induction and protein expression. In contrast, STAT-3 activation was positively correlated with p21 protein expression in both groups of mice. Because these results link exaggerated STAT-3 activation with impaired hepatocyte proliferation, STAT-3 inhibition cannot be a growth-arrest mechanism in ob/ob fatty livers. Rather, hyperinduction of this factor may promote mitoinhibition by up-regulating mechanisms that impede cell cycle progression.
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