ArticleLaboratory investigation; a journal of technical methods and pathology2016
Tim-4 protects mice against lipopolysaccharide-induced endotoxic shock by suppressing the NF-κB signaling pathway.
Article in Laboratory investigation; a journal of technical methods and pathology, 2016. 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, 17 citations in OpenAlex.
- Up-regulation of blood-circulating TIM-4-expressing monocytes and potential diagnostic biomarker sTIM-4 in primary liver cancer.Scientific reports · 2025Article
- IRG1/itaconate enhances efferocytosis by activating Nrf2-TIM4 signaling pathway to alleviate con A induced autoimmune liver injury.Cell communication and signaling : CCS · 2025Article
- Macrophage Tim-4 protects against deep vein thrombosis by binding CK2β to suppress inflammatory responses.Frontiers in immunology · 2025Article
- Whole-Transcriptome Analysis Reveals the Regulatory Network of Immune Response in Dapulian Pig.Animals : an open access journal from MDPI · 2024Article
- Tim-4 alleviates acute hepatic injury by modulating homeostasis and function of NKT cells.Clinical and experimental immunology · 2024Article
- Function and characteristics of TIM‑4 in immune regulation and disease (Review).International journal of molecular medicine · 2023Review
- T-Cell Immunoglobulin and Mucin Domain-Containing Protein-4 Is Critical for Kupffer Cell Homeostatic Function in the Activation and Resolution of Liver Ischemia Reperfusion Injury.Hepatology (Baltimore, Md.) · 2021Article
- IL-6 promotes metastasis of non-small-cell lung cancer by up-regulating TIM-4 via NF-κB.Cell proliferation · 2020Article
- Tim-4 in Health and Disease: Friend or Foe?Frontiers in immunology · 2020Review
- PI3K/Akt pathway-mediated HO-1 induction regulates mitochondrial quality control and attenuates endotoxin-induced acute lung injury.Laboratory investigation; a journal of technical methods and pathology · 2019Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotoxic shock is the primary cause of morbidity and mortality in hospital patients, creating an urgent need to explore the mechanisms involved in sepsis. Our previous studies showed that T-cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4) attenuated the inflammatory response through regulating the functions of macrophages. However, the mechanism by which Tim-4 does this has not been fully elucidated. In this study, we found that Tim-4 expression was increased in lipopolysaccharide (LPS)-induced endotoxic shock. Interestingly, the survival rate of mice in the Tim-4 overexpression group was higher than that of the control group after LPS administration. To investigate the function of Tim-4 in LPS-induced inflammation, we further demonstrated that Tim-4 attenuated LPS-induced endotoxic shock by inhibiting cytokine production by macrophages. Blocking expression of Tim-4 and nuclear factor-kappa B (NF-κB) signal inhibition showed that Tim-4 inhibited cytokine production via NF-κB signaling pathway. This study indicates that Tim-4 may exert its immune modulation by regulating inflammatory factor secretion and might act as a novel potential target for inflammatory diseases, especially endotoxic shock.
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