ArticleCell death & disease2021
Glucocorticoid-induced leucine zipper regulates liver fibrosis by suppressing CCL2-mediated leukocyte recruitment.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
- Coordinated Two-Node Blockade of NF-κB and TGF-β/Smad Signaling Attenuates the Foreign Body Response to Prevent Capsular Contracture.Biomedicines · 2026Article
- Novel Insights into TSC22D Family Genes in Metabolic Diseases and Cancer.Biomolecules · 2026Review
- Effective Components and Molecular Mechanism of Biejiaruangan Capsule Against Liver Fibrosis: High-resolution Mass Spectrometry, Network Pharmacological Analysis and Experimental Verification.Combinatorial chemistry & high throughput screening · 2026Article
- Glucocorticoid-induced leucine zipper as a context-dependent central integrator of innate and adaptive immune homeostasis.Frontiers in immunology · 2026Review
- L-GILZ is essential for cardiac function and protects against pressure overload-induced hypertrophy and dysfunction in mice.Asian heart journal · 2025Article
- Macrophage migration inhibitory factor in inflammasome formation and macrophage recruitment by cervical squamous cell carcinoma cells.Oncology letters · 2025Article
- Identification and Validation of a New Functional GeneStem cells international · 2025Article
- TIMP-1 Promotes Expression of MCP-1 and Macrophage Migration by Inducing Fli-1 in Experimental Liver Fibrosis.Journal of clinical and translational hepatology · 2024Article
- Macrophages promote the transition from myocardial ischemia reperfusion injury to cardiac fibrosis in mice through GMCSF/CCL2/CCR2 and phenotype switching.Acta pharmacologica Sinica · 2024Article
- Channel Expansion in the Ligand-Binding Domain of the Glucocorticoid Receptor Contributes to the Activity of Highly Potent Glucocorticoid Analogues.Molecules (Basel, Switzerland) · 2024Article
- Immunomodulation by glucocorticoid-induced leucine zipper in macrophages: enhanced phagocytosis, protection from pyroptosis, and altered mitochondrial function.Frontiers in immunology · 2024Article
- Single-cell transcriptomic analysis reveals heterogeneous features of myeloid-derived suppressor cells in newborns.Frontiers in immunology · 2024Article
- The role and therapeutic targeting of the CCL2/CCR2 signaling axis in inflammatory and fibrotic diseases.Frontiers in immunology · 2024Review
- Dynamic RBM47 ISGylation confers broad immunoprotection against lung injury and tumorigenesis via TSC22D3 downregulation.Cell death discovery · 2023Article
- Role of histamine HInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Article
- High-fat diet in early life triggers both reversible and persistent epigenetic changes in the medaka fish (Oryzias latipes).BMC genomics · 2023Article
- Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis (LF) is a dangerous clinical condition with no available treatment. Inflammation plays a critical role in LF progression. Glucocorticoid-induced leucine zipper (GILZ, encoded in mice by the Tsc22d3 gene) mimics many of the anti-inflammatory effects of glucocorticoids, but its role in LF has not been directly addressed. Here, we found that GILZ deficiency in mice was associated with elevated CCL2 production and pro-inflammatory leukocyte infiltration at the early LF stage, resulting in enhanced LF development. RNA interference-mediated in vivo silencing of the CCL2 receptor CCR2 abolished the increased leukocyte recruitment and the associated hepatic stellate cell activation in the livers of GILZ knockout mice. To highlight the clinical relevance of these findings, we found that TSC22D3 mRNA expression was significantly downregulated and was inversely correlated with that of CCL2 in the liver samples of patients with LF. Altogether, these data demonstrate a protective role of GILZ in LF and uncover the mechanism, which can be targeted therapeutically. Therefore, modulating GILZ expression and its downstream targets represents a novel avenue for pharmacological intervention for treating LF and possibly other liver inflammatory disorders.
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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.