Glucocorticoids have opposing effects on liver fibrosis in hepatic stellate and immune cells
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Liver fibrosis is a reversible wound-healing process that is protective in the short term, but prolonged fibrotic responses lead to excessive accumulation of extracellular matrix components that suppresses hepatocyte regeneration, resulting in permanent liver damage. Upon liver damage, nonparenchymal cells including immune cells and hepatic stellate cells (HSCs) have crucial roles in the progression and regression of liver fibrosis. Here, we report differential roles of the glucocorticoid receptor (GR), acting in immune cells and HSCs, in liver fibrosis. In the carbon tetrachloride hepatotoxin-induced fibrosis model, both steroidal and nonsteroidal GR ligands suppressed expression of fibrotic genes and decreased extracellular matrix deposition but also inhibited immune cell infiltration and exacerbated liver injury. These counteracting effects of GR ligands were dissociated in mice with conditional GR knockout in immune cells (GRLysM) or HSC (GRhGFAP): the impacts of dexamethasone on immune cell infiltration and liver injury were totally blunted in GRLysM mice, whereas the suppression of fibrotic gene expression was diminished in GRhGFAP mice. The effect of GR activation in HSC was further confirmed in the LX-2 HSC cell line, in which antifibrotic effects were mediated by GR ligand inhibition of Sma and mad-related protein 3 (SMAD3) expression. We conclude that GR has differential roles in immune cells and HSCs to modulate liver injury and liver fibrosis. Specific activation of HSC-GR without alteration of GR activity in immune cells provides a potential therapeutic approach to treatment of hepatic fibrosis.
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Kim et al. suggested that the impact of GR activation is likely mediated by repressing NF-κB, SMAD3 and AP-1, thus demonstrating anti-inflammatory and possibly anti-fibrotic effects.
“Kim et al. suggested that the impact of GR activation is likely mediated by repressing NF-κB, SMAD3 and AP-1, thus demonstrating antiinflammatory and possibly anti-fibrotic effects.[197]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [197]
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Nanomedicine-Driven Modulation of Signaling Pathways in Hepatic Fibrosis
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Endocrine determinants of MASLD: mechanisms and therapeutic targets
Chaturvedi, R., Mathew, A., Pradhan, A., Goyal, M., Sharma, M., Kachroo, V., Agrawal, C., Krishnamurthy, A., Atreja, S. M., & Atreja, A. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2026.1967494
- Authors
- Kim, K. H., Lee, J. M., Zhou, Y., Harpavat, S., & Moore, D. D.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Moore, David D.
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2016-08-01
- Volume
- 30
- Issue
- 8
- Pages
- 905-916
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- PMC
- PMC5414623
- OpenAlex
- W2474249973
- Cited by
- 41
- References
- 62
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 8 · 2023: 5 · 2022: 5 · 2021: 4 · 2020: 4 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 1
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- liver fibrosis, glucocorticoid receptor, hepatic stellate cells, immune cells, dexamethasone, carbon tetrachloride hepatotoxicity, extracellular matrix deposition, Smad3, immune cell infiltration, liver injury, antifibrotic therapy
- MeSH terms
- Animals, Carbon Tetrachloride, Cell Line, Cells, Cultured, Glucocorticoids, Humans, Immunohistochemistry, Liver, Liver Cirrhosis, Lymphocytes, Macrophages, Mice, Inbred C57BL, Monocytes, Receptors, Glucocorticoid, Signal Transduction, Mice, Knockout, RNA, Small Interfering, Mice, Hepatic Stellate Cells, Chemical and Drug Induced Liver Injury, Real-Time Polymerase Chain Reaction
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