ArticleCellular and molecular gastroenterology and hepatology2026
Hepatic Arterial Flow-Induced Portal Tract Fibrosis in Portal Hypertension: The Role of VCAM-1 and Osteopontin-Expressing Macrophages.
Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Endothelial cell glycogen synthase kinase 3β promotes lipotoxic endotheliopathy and liver inflammation in MASH.JCI insight · 2026Article
- Unveiling the Immunopharmacological Mechanisms of Biejiajian Pills (BJJP) Underlying the Treatment of Hepatic Fibrosis: Insights From Network Pharmacology and Experimental Validation.Food science & nutrition · 2026Article
- Hemodynamics and matrix stiffness shape the pathogenicity of SPP1Frontiers in immunology · 2026Review
- VCAM-1 and Osteopontin Link Hemodynamic Alteration to Fibrosis in Portal Hypertension.Cellular and molecular gastroenterology and hepatology · 2026Article
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11 authors.
Funding
Abstract
BACKGROUND &
aimsThe liver undergoes significant hemodynamic changes during surgery, transplantation, or cirrhosis with portal hypertension (PH). The hepatic artery buffer response (HABR), which compensates for reduced portal venous flow by increasing hepatic artery (HA) flow, is hypothesized to induce pathological portal tract remodeling. This study investigates the molecular mechanisms underlying this process.
methodsPH was induced in Sprague-Dawley rats via partial portal vein ligation (PPVL). Structural evaluation (micro computed tomography [microCT]), immune cell profiling, hemodynamic measurements, and transcriptomic analysis in macrophages from sham or PPVL rats were conducted.
resultsMicroCT revealed decreased portal vein flow and increased HA flow correlated with portal pressure (r = 0.799; P < .01). A 2-fold increase in portal tract fibrosis (P < .001) was observed with increased alpha smooth muscle actin (α-SMA)+ myofibroblasts in PPVL rats. CD68
conclusionsIncreased VCAM-1 in arterial endothelial cells and PFs facilitates the recruitment of Spp1
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