ArticleThe Journal of biological chemistry2016
Glucocorticoid Induces Hepatic Steatosis by Inhibiting Activating Transcription Factor 3 (ATF3)/S100A9 Protein Signaling in Granulocytic Myeloid-derived Suppressor Cells.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease.Lipids in health and disease · 2025Pooled it
- Circulating M-MDSC Expansion During Therapy Associates With Treatment Response in Multiple Myeloma: A Longitudinal Observational Study.Clinical and translational science · 2026Observational
- Loss of adipose ATF3 promotes adipose tissue lipolysis and the development of MASH.Communications biology · 2024Article
- Article
- Article
- Neutrophils and lymphopenia, an unknown axis in severe COVID-19 disease.PLoS pathogens · 2021Article
- Dexamethasone and lactoferrin induced PMN-MDSCs relieved inflammatory adverse events of anti-cancer therapy without tumor promotion.Communications biology · 2021Article
- Methylprednisolone alleviates multiple sclerosis by expanding myeloid-derived suppressor cells via glucocorticoid receptor β and S100A8/9 up-regulation.Journal of cellular and molecular medicine · 2020Article
- Liposomal Delivery Improves the Efficacy of Prednisolone to Attenuate Renal Inflammation in a Mouse Model of Acute Renal Allograft Rejection.Transplantation · 2020Article
- Modulation of Immunosuppression by Oligonucleotide-Based Molecules and Small Molecules Targeting Myeloid-Derived Suppressor Cells.Biomolecules & therapeutics · 2020Review
- Master Regulator Activating Transcription Factor 3 (ATF3) in Metabolic Homeostasis and Cancer.Frontiers in endocrinology · 2020Review
- Transcriptional factor ATF3 protects against colitis by regulating follicular helper T cells in Peyer's patches.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Dual-release hydrocortisone improves hepatic steatosis in patients with secondary adrenal insufficiency: a real-life study.Therapeutic advances in endocrinology and metabolism · 2019Article
- Prognostic values of S100 family members in ovarian cancer patients.BMC cancer · 2018Article
- Expansion and activation of monocytic-myeloid-derived suppressor cell via STAT3/arginase-I signaling in patients with ankylosing spondylitis.Arthritis research & therapy · 2018Article
- Role of activating transcription factor 3 in fructose-induced metabolic syndrome in mice.Hypertension research : official journal of the Japanese Society of Hypertension · 2018Article
- Activating transcription factor 3 in immune response and metabolic regulation.Liver research (Beijing, China) · 2017Article
- Use antibiotics in cell culture with caution: genome-wide identification of antibiotic-induced changes in gene expression and regulation.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoids (GCs) used as inflammation suppressors have harmful side effects, including induction of hepatic steatosis. The underlying mechanisms of GC-promoted dysregulation of lipid metabolism, however, are not fully understood. GCs could facilitate the accumulation of myeloid-derived suppressor cells (MDSC) in the liver of animals, and the potential role of MDSCs in GC-induced hepatic steatosis was therefore investigated in this study. We demonstrated that granulocytic (G)-MDSC accumulation mediated the effects of GCs on the fatty liver, in which activating transcription factor 3 (ATF3)/S100A9 signaling plays an important role. ATF3-deficient mice developed hepatic steatosis and displayed expansion of G-MDSCs in the liver and multiple immune organs, which shared high similarity with the phenotype observed in GC-treated wild-type littermates. Adoptive transfer of GC-induced or ATF3-deficient G-MDSCs promoted lipid accumulation in the liver, whereas depletion of G-MDSCs alleviated these effects. Mechanistic studies showed that in MDSCs, ATF3 was transrepressed by the GC receptor GR through direct binding to the negative GR-response element. S100A9 is the major transcriptional target of ATF3 in G-MDSCs. Silencing S100A9 clearly alleviated G-MDSCs expansion and hepatic steatosis caused by ATF3 deficiency or GC treatment. Our study uncovers an important role of G-MDSCs in GC-induced hepatic steatosis, in which ATF3 may have potential therapeutic implications.
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