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Therapeutic Activity of Resolvin D1 (RvD1) in Murine MASH
Amaia Navarro-Corcuera1, Yiwei Zhu1, Fanglin Ma1
1Division of Liver Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Biorxiv : the Preprint Server for Biology
|May 7, 2024
Summary
Resolvin D1 (RvD1) combats metabolic dysfunction-associated steatohepatitis (MASH) by reducing inflammation and liver fibrosis. This study uncovers RvD1's protective mechanisms against MASH progression.
Area of Science:
- Hepatology
- Immunology
- Molecular Biology
Background:
- Metabolic dysfunction-associated steatohepatitis (MASH) is a growing health concern with limited therapeutic options.
- Resolvin D1 (RvD1), a docosahexaenoic acid (DHA)-derived mediator, shows promise in mitigating MASH, but its mechanisms remain unclear.
Approach:
- Investigated RvD1's effects in a murine MASH model using bulk and single-cell RNA sequencing.
- Analyzed primary cells (macrophages, T cells, hepatocytes) to understand RvD1's impact on inflammation, cell death, and fibrosis.
- Examined RvD1 levels in human MASH tissues.
Key Points:
- Hepatic RvD1 levels are reduced in MASH, linked to pro-inflammatory macrophage expansion.
- RvD1 administration suppressed Stat1-Cxcl10 signaling in macrophages, reducing inflammation.
- RvD1 alleviated ER stress-induced apoptosis in hepatocytes.
- RvD1 modulated matrix metalloproteinase (MMP) expression in hepatic stellate cells and macrophages, promoting fibrosis regression.
Conclusions:
- RvD1 effectively reduces inflammation, hepatocyte apoptosis, and liver fibrosis in MASH.
- RvD1 acts through Stat1-mediated inflammation suppression, ER stress mitigation, and MMP-driven fibrosis regression.
- RvD1 demonstrates significant therapeutic potential for treating MASH.
