Stimulating healthy tissue regeneration by targeting the 5-HT2B receptor in chronic liver disease
Open accessAbstract
Tissue homeostasis requires an effective, limited wound-healing response to injury. In chronic disease, failure to regenerate parenchymal tissue leads to the replacement of lost cellular mass with a fibrotic matrix. The mechanisms that dictate the balance of cell regeneration and fibrogenesis are not well understood. Here we report that fibrogenic hepatic stellate cells (HSCs) in the liver are negative regulators of hepatocyte regeneration. This negative regulatory function requires stimulation of the 5-hydroxytryptamine 2B receptor (5-HT(2B)) on HSCs by serotonin, which activates expression of transforming growth factor β1 (TGF-β1), a powerful suppressor of hepatocyte proliferation, through signaling by mitogen-activated protein kinase 1 (ERK) and the transcription factor JunD. Selective antagonism of 5-HT(2B) enhanced hepatocyte growth in models of acute and chronic liver injury. We also observed similar effects in mice lacking 5-HT(2B) or JunD or upon selective depletion of HSCs in wild-type mice. Antagonism of 5-HT(2B) attenuated fibrogenesis and improved liver function in disease models in which fibrosis was pre-established and progressive. Pharmacological targeting of 5-HT(2B) is clinically safe in humans and may be therapeutic in chronic liver disease.
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HSC depletion with lower potency and specificity, using gliotoxin or GFAP-TK, has yielded inconsistent effects on liver regeneration and injury.
“HSC depletion with lower potency and specificity, using gliotoxin or GFAP-TK, has yielded inconsistent effects on liver regeneration and injury15–18.”
From Hepatic stellate cells control liver zonation, size and functions via R-spondin 3 (2025) · cites this paper as [15]
The paper’s main text (indexed under Abstract; page unavailable) reports HSC depletion using C1-3–gliotoxin and increased hepatocyte proliferation. It does not discuss GFAP-TK or establish that these methods have lower potency and specificity or have yielded inconsistent effects on regeneration and injury. (LLM, conf=0.82)
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- Authors
- Ebrahimkhani, M. R., Oakley, F., Murphy, L. B., Mann, J., Moles, A., Perugorria, M. J., Ellis, E., Lakey, A. F., Burt, A. D., Douglass, A., Wright, M. C., White, S. A., Jaffré, F., Maroteaux, L., & Mann, D. A.
- Affiliations
- Newcastle University (GB)
- Inserm (FR)
- Corresponding author
- Mann, Derek A
- ORCID
- Venue
- Nature Medicine
- Published
- 2011-11-27
- Volume
- 17
- Issue
- 12
- Pages
- 1668-1673
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3428919
- OpenAlex
- W2065840120
- Cited by
- 221
- References
- 34
- Citations by year
- 2026: 14 · 2025: 11 · 2024: 11 · 2023: 10 · 2022: 12 · 2021: 19 · 2020: 20 · 2019: 15 · 2018: 16 · 2017: 16 · 2016: 19 · 2015: 12 · 2014: 14 · 2013: 20 · 2012: 12
- FWCI
- 8.85
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- Wellcome Trust (086755, WT086755MA, 82439, WT084961MA)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Keywords
- 5-HT2B receptor, serotonin signaling, hepatic stellate cells, liver fibrosis, hepatocyte regeneration, chronic liver disease, TGF-β1, ERK signaling, JunD, wound healing, tissue regeneration
- MeSH terms
- Animals, Cells, Cultured, Chronic Disease, Electrophoresis, Polyacrylamide Gel, Immunohistochemistry, Indoles, Liver Cirrhosis, Male, Mice, Inbred C57BL, Serotonin, Urea, Wound Healing, Signal Transduction, Proto-Oncogene Proteins c-jun, Rats, Sprague-Dawley, Mice, Knockout, Mitogen-Activated Protein Kinase 1, Hepatocytes, Receptor, Serotonin, 5-HT2B, Cell Proliferation, Mice, Rats, Transforming Growth Factor beta1, Hepatic Stellate Cells, Serotonin 5-HT2 Receptor Antagonists
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