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The Spleen Promotes Liver Sinusoidal Endothelial Cell Angiogenesis by Stimulating the TGFβ/Smad2/3 Pathway Through
Xi Deng1,2, Na Huang1,2, Ke Du1,2
1National & Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Journal of Gastroenterology and Hepatology
|January 5, 2026
Summary
The spleen promotes liver sinusoidal endothelial cell (LSEC) angiogenesis in liver fibrosis. Spleen serum elevates Growth Differentiation Factor 15 (GDF15), activating the TGFβ/Smad2/3 pathway to enhance LSEC functions.
Area of Science:
- Hepatology
- Vascular Biology
- Cellular Signaling
Background:
- Liver sinusoidal endothelial cells (LSECs) are critical in liver fibrosis progression.
- The spleen's role in LSEC function during fibrosis is not fully understood.
- Chronic liver diseases can lead to pathological progression associated with the spleen.
Purpose of the Study:
- To investigate the spleen's effect on LSEC angiogenesis.
- To elucidate the underlying mechanisms of spleen-mediated LSEC modulation in liver fibrosis.
Main Methods:
- Splenectomy was performed on CCl4-induced liver fibrosis mice.
- Cultured LSECs were treated with serum from cirrhotic patients (pre- and post-splenectomy) and controls.
- LSEC proliferation, migration, tubule formation, and signaling pathways (TGFβ/Smad2/3) were assessed.
Main Results:
- The spleen significantly promoted LSEC angiogenesis in fibrotic models.
- Spleen serum from cirrhotic patients enhanced LSEC proliferation, migration, and tubule formation.
- Growth Differentiation Factor 15 (GDF15) in spleen serum was identified as a key mediator, activating Smad2/3 phosphorylation and promoting angiogenesis.
Conclusions:
- The spleen promotes LSEC angiogenesis during liver fibrosis.
- This effect is mediated by GDF15 in spleen serum.
- GDF15 activates the TGFβ/Smad2/3 pathway in LSECs, driving pro-angiogenic effects.
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