ArticleCell proliferation2020
TIM-4 interference in Kupffer cells against CCL4-induced liver fibrosis by mediating Akt1/Mitophagy signalling pathway.
Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 87 citations in OpenAlex.
- Emerging roles of mitophagy in liver fibrosis: Implications for therapy.Acta pharmacologica Sinica · 2026Review
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- 3-carbamoyl proxyl nitroxide attenuates CClScientific reports · 2026Article
- An autoimmunity-associated allele ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Development and external validation of a mitophagy-related diagnostic model for biliary atresia based on cellular infiltration patterns.Translational pediatrics · 2026Article
- Hepatocyte-Derived Apoptotic Bodies as Pathological Intercellular Messengers in the Liver.Biomolecules · 2026Review
- Taohong Siwu Decoction relieves renal fibrosis: based on network pharmacology and experimental confirmation.Renal failure · 2025Article
- Resveratrol ameliorates CClMolecular biology reports · 2025Article
- An Autoimmunity-associated allele ofbioRxiv : the preprint server for biology · 2025Article
- Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025Review
- Integrated analyses to explore the mechanism of Gancao Renshen Zhixue Decoction in treating liver cirrhosis.Scientific reports · 2025Article
- Article
- Novel regulators of hepatic macrophages in liver fibrosis.Frontiers in immunology · 2025Review
- The impact of diet-induced obesity on 5 fluorouracil-induced tumor and liver immune cell cytotoxicity.American journal of physiology. Cell physiology · 2025Article
- TIM4+macrophages suppress the proinflammatory response to maintain the chronic alveolar echinococcosis infection.Frontiers in cellular and infection microbiology · 2025Article
- Mechanism Study of Xiaoyao San against Nonalcoholic Steatohepatitis-Related Liver Fibrosis Based on a Combined Strategy of Transcriptome Analysis and Network Pharmacology.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Liver Cell Mitophagy in Metabolic Dysfunction-Associated Steatotic Liver Disease and Liver Fibrosis.Antioxidants (Basel, Switzerland) · 2024Review
- Macrophage Perspectives in Liver Diseases: Programmed Death, Related Biomarkers, and Targeted Therapy.Biomolecules · 2024Review
- The pivotal role of dysregulated autophagy in the progression of non-alcoholic fatty liver disease.Frontiers in endocrinology · 2024Review
- Network Pharmacology, Molecular Docking Analysis and Molecular Dynamics Simulation ofCurrent pharmaceutical design · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesT-cell immunoglobulin domain and mucin domain-4 (TIM-4) is selectively expressed on antigen-presenting cells (APCs) and modulates various immune responses. However, the role of TIM-4 expressed by Kupffer cells (KCs) in liver fibrosis remains unclear. The present study aimed to explore whether and how TIM-4 expressed by KCs is involved in liver fibrosis. MATERIALS AND
methodsMice chronic liver fibrosis models were established and divided into the olive-induced control group, CCL4-induced control group, olive-induced TIM-4 interference group and CCL4-induced TIM-4 interference group. Different techniques were used to monitor the fibrotic effects of TIM-4, including histopathological assays, Western blotting, ELISA and transmission electron microscopy. Additionally, mice liver transplant models were established to determine the fibrotic effects of TIM-4 on fibrosis after liver transplantation (LT).
resultsWe found that the induction of liver fibrosis by CCL4 was associated with TIM-4 expression in KCs. TIM-4 interference essentially contributed to liver fibrosis resolution. KCs from the TIM-4 interference group had decreased levels of pro-fibrotic markers, reduced TGF-β1 secretion and inhibited hepatic stellate cell (HSC) differentiation into myofibroblast-like cells. In addition, we used GdCl3 to verify that KCs are the primary source of TGF-β1 during fibrosis progression. Moreover, KCs from CCL4-induced mice showed increased ROS production, mitophagy activation and TGF-β1 secretion. However, TIM-4 interference in the KCs inhibited Akt1-mediated ROS production, resulting in the suppression of PINK1, Parkin and LC3-II/I activation and the reduction of TGF-β1 secretion during liver fibrosis. Additionally, TIM-4 interference potentially attenuated development of fibrosis after LT.
conclusionsOur findings revealed the underlying mechanisms of TIM-4 interference in KCs to mitigate liver fibrosis.
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