Young-Ri Shim, Hee-Hoon Kim, Min Jeong Kim, Jun-Hee Lee, Kyurae Kim, Sung Eun Choi, Katherine Po Sin Chung, Eunmi Lee, Kwang Woo Lee, Jihyo Byun, Jaewoo Oh, Jae Min Han, Jun Ho Byun, Jong-Eun Park, Won Kim, Young-Sun Lee, Won-Il Jeong
Received April 5, 2026 Accepted June 16, 2026 Published online June 18, 2026
Background/Aims Bone marrow mesenchymal stromal cells (BM-MSCs) exert diverse functions, including supporting alcohol detoxification and providing a niche for monocyte development. However, their role in regulating monocytes during alcohol-related liver disease (ALD) remains unclear. This study investigates how BM-MSCs orchestrate the egress of anti-inflammatory monocytes from BM to the liver in ALD.
Methods Wild-type, leptin receptor (LepR)⁺ BM-MSC-specific Slc7a11 knockout, and natural killer (NK) cell-specific Grm5 knockout mice were fed an ethanol diet for 8 weeks. Tissue analyses were performed using single-cell RNA sequencing (scRNA-seq), immunostaining, and flow cytometry. Blood and liver samples from ALD patients were examined.
Results scRNA-seq revealed a distinct population of BM-derived Ly6Clow hepatic macrophages expressing interleukin-1 receptor 2 (IL-1R2), an IL-1β decoy receptor, in ethanol-fed mice. In the BM, alcohol exposure upregulated the gene expression of alcohol-metabolizing enzymes (Adh1, Aldh2), xCT (Slc7a11), and chemokines (Cxcl9, Cxcl10) in LepR+ BM-MSCs, promoting NK cell recruitment and interferon-γ (IFN-γ) production via metabotropic glutamate receptor 5 (mGluR5) activation. Subsequently, IFN-γ enhanced IL-1R2 expression and suppressed CX3CR1 in neighboring Ly6Clow BM monocytes, facilitating their hepatic migration. LepR+ BM-MSC-specific xCT and NK cell-specific mGluR5 knockout mice exhibited exacerbated liver injury and elevated blood IL-1β levels, while recombinant IL-1R2 administration improved ameliorated ALD in wild-type mice. Consistently, increased IL-1R2 levels were observed in plasma, CD14+CD16+ blood monocytes, and liver tissues of ALD patients.
Conclusions We identified a BM-liver axis in which glutamate released by BM-MSCs activates mGluR5 in BM NK cells, driving IL-1R2+ monocyte migration to the liver and attenuating ALD progression.
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Background/Aims Sarcopenia negatively affects the prognosis of cirrhotic patients, but clinical implications of changes in muscle mass remain unclear. We aimed to elucidate its role in the prognosis of outpatients with cirrhosis.
Methods Patients with cirrhosis who underwent annual abdominal computed tomography (CT) for hepatocellular carcinoma surveillance were included in the prospective cohort. The L3 skeletal muscle index (SMI) was adopted as a proxy for the amount of skeletal muscle, and the rate of SMI change between inclusion and after 1 year (ΔSMI/yr%) was calculated.
Results In total, 595 patients underwent a second CT after 1 year. Among them, 109 and 64 patients had sarcopenia and Child-Pugh class B/C decompensation at inclusion, which changed to 103 and 45 at the 1-year follow-up, respectively. During a median follow-up of 30.1 months after 1 year, 86 patients had at least one cirrhosis complication, and 18 died or received liver transplantation. In the development of cirrhosis complications, ΔSMI/yr% was independently associated, even after adjusting for the Child-Pugh and model for end stage liver disease (MELD)-Na scores. In addition, ΔSMI/yr% showed a good predictive performance for the development of cirrhosis complications within 6 months after 1-year follow-up in all subgroups, with a cut-off of -2.62 (sensitivity, 83.9%; specificity, 74.5%) in the overall population. SMI at 1-year and Child-Pugh score were independent factors associated with survival. In addition, changes in sarcopenia status significantly stratified survival.
Conclusion ΔSMI/yr% was a good predictor of the development of cirrhosis complications in outpatients with cirrhosis, independent of Child-Pugh and MELD scores.
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Background/Aims Useful biomarkers for metabolic syndrome have been insufficient. We investigated the performance of serum milk fat globule-EGF factor-8 (MFG-E8), the key mediator of inflammatory pathway, in diagnosis of metabolic syndrome.
Methods Subjects aged between 30 and 64 years were prospectively enrolled in the Seoul Metabolic Syndrome cohort. Serum MFG-E8 levels were measured at baseline.
Results A total of 556 subjects were included, comprising 279 women (50.2%) and 277 men (49.8%). Metabolic syndrome was diagnosed in 236 subjects (42.4%), and the mean MFG-E8 level of subjects with metabolic syndrome was significantly higher than that of subjects without metabolic syndrome (P<0.001). MFG-E8 level was significantly correlated with all metabolic syndrome components and pulse wave velocity (all P<0.05). Subjects were categorized into two groups according to the best MFG-E8 cut-off value as follows: group 1, MFG-E8 level <4,745.1 pg/mL (n=401, 72.1%); and group 2, MFG-E8 level ≥4,745.1 (n=155, 27.9%). At baseline, metabolic syndrome in group 2 was significantly more prevalent than in group 1 (63.9% vs. 34.2%, P<0.001). During median follow-up of 17 months, metabolic syndrome developed in 122 (38.1%) subjects among 320 subjects without it at baseline. The incidence of metabolic syndrome in group 2 was significantly higher than that in group 1 (55.4% vs. 34.5%, P=0.003). On multivariate analysis, MFG-E8 level ≥4,745.1 pg/mL was an independent predictor for diagnosis and development of metabolic syndrome after adjusting other factors (all P<0.05).
Conclusions Serum MFG-E8 level is a potent biomarker for the screening and prediction of metabolic syndrome.
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Since sorafenib was introduced in 2007 for treating advanced hepatocellular carcinoma (HCC), 15 patients have achieved a complete response (CR) in advanced HCC. However, only four of these reports can be regarded as real CRs involving adequate assessments including imaging, serum tumor markers, and histologic examinations of completely resected specimens. A 54-year-old man with hepatitis C virus (HCV)-related liver cirrhosis (LC) presented to our unit. A CT scan demonstrated a 3.8-cm arterial hypervascular/portal-washout mass in the right lobe and invasion in the right portal vein. Twelve weeks after beginning sorafenib therapy, the AFP level was normalized and a CT scan showed a prominent decrease in the hepatic mass and a significant decrease in the volume of portal vein thrombosis (PVT). The patient received a right liver hemihepatectomy after 12 months. No viable tumor cells were found in the resected specimen, and there was no thrombotic obstruction of the portal vein. Twelve months later the patient showed no clinical evidence of HCC recurrence. This is the first case of CR in HCC treatment following sorafenib with histologically confirmed HCVrelated HCC without LC evidence, HCC with PVT, and a follow-up of longer than 12 months. This case seems to be an extremely unusual clinical outcome in advanced HCC.
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