Metabolism-associated fatty liver disease (MAFLD) is a disease of hepatic fat accumulation resulting from metabolic disorders. Currently, MAFLD is the most common cause of chronic liver disease in children and adolescents. No effective or safe drugs for treating children with MAFLD are available. The traditional Chinese medicine used for treating MAFLD in children is characterized by being holistically regulated, multileveled, multi-targeting, and very safe. In this paper, the progress in research involving treatment using traditional Chinese medicine for MAFLD in children is reviewed.

End-stage liver disease (ESLD) is characterized by a dramatic deterioration of liver function, frequently accompanied by systemic inflammatory storms and multiple organ failures. Central to the onset and progression of ESLD, systemic inflammation arises from complex interactions among various inflammatory signaling molecules and immune cells within and beyond the liver. As key inflammatory modulatory molecules, bioactive oxylipins have been increasingly recognized for their complex molecular mechanisms implicated in various diseases. This review aims to summarize recent findings regarding the molecular and immunological mechanisms through which oxylipins contribute to the development of liver injury and failure, with emphasis on both substantial intrahepatic and extrahepatic immune and inflammatory dysregulation associated with ESLD. Furthermore, this review discusses the translational potential of targeting oxylipins for clinical diagnosis, prognosis, and therapeutic intervention in ESLD.

This Consensus aims to establish a physician–pharmacist co-management model to standardize the rational clinical application of anti-immunoglobulin E monoclonal antibodies in the treatment of allergic asthma. Focusing on the critical components of physician–pharmacist co-management, key issues related to anti-immunoglobulin E monoclonal antibody therapy were identified through a systematic literature review and clinical practice experience. Evidence quality was evaluated using an evidence grading system, and the Delphi method was applied to reach expert consensus. Centered on omalizumab, the Consensus presents 12 recommendations covering the work model of physician–pharmacist co-management, clinical management pathways, hierarchical diagnosis and treatment systems, as well as training and competency assessment. The Delphi process achieved a high degree of consensus (agreement >80%) on 12 key recommendations, emphasizing a 60-min observation period post-injection and quarterly follow-up evaluations. It establishes a standardized framework for the co-management of omalizumab therapy in allergic asthma. Results highlighted that co-management effectively monitors omalizumab dosage (75–600 mg) and maintains a consensus threshold of >80% for patient safety protocols. The Consensus provides a standardized framework for physician–pharmacist co-management, which is expected to facilitate rational drug use and improve patient care pathways in omalizumab therapy.

Hepatic ischemia–reperfusion (HIR) injury impairs outcomes post–liver transplantation. Therefore, we aimed to investigate the role and mechanism of miR-381-3p in HIR.

The study enrolled 150 healthy controls, 82 non-HIR-injured patients, and 68 patients with HIR injury following liver transplantation. Clinical data were analyzed. Multivariate analysis identified HIR risk factors; the predictive value of miR-381-3p was assessed via receiver operating characteristic analysis. An in vitro hypoxia/reoxygenation (H/R) model was established and employed. The cellular effects of miR-381-3p and JAK2 were evaluated using CCK-8, flow cytometry, ELISA, luciferase, RIP, and bioinformatics.

Serum miR-381-3p was significantly elevated in HIR compared with the other groups. miR-381-3p was the strongest independent HIR risk factor, which was confirmed by receiver operating characteristic analysis. H/R upregulated miR-381-3p. Inhibiting miR-381-3p counteracted H/R-induced decreased viability and increased apoptosis, inflammation, and oxidative stress. miR-381-3p directly bound to and suppressed JAK2 via its 3′ untranslated region (validated by luciferase and RIP). Transfection of si-JAK2 abolished the protective effects of miR-381-3p inhibition.

miR-381-3p exacerbates post-transplant HIR by directly targeting JAK2, amplifying inflammation and oxidative stress. Thus, our findings nominate serum miR-381-3p as a promising non-invasive biomarker and suggest its potential as a therapeutic target for mitigating HIR injury.

Terahertz (THz) radiation is increasingly explored for biomedical applications, however, its non-thermal effects on cellular metabolism and regulatory networks remain insufficiently characterized. This study aimed to investigate how 2.3 THz radiation affects metabolic pathways and membrane-associated signaling in human melanoma cells.

SK-MEL-28 melanoma cells were exposed to 2.3 THz radiation for 45 min using the 1st Novosibirsk free-electron laser. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and trypan blue assays. Metabolic alterations were detected by targeted metabolomics using liquid chromatography–tandem mass spectrometry. Gene network analysis was performed using the ANDSystem platform to reconstruct gene and protein interaction networks linking altered metabolites to membrane receptors, lipid raft proteins, and signaling pathways. Overrepresentation analysis of biological processes was applied to identify enriched functional categories.

THz exposure did not affect cell viability but induced significant alterations in purine metabolism, pantothenate/CoA biosynthesis, and the pentose phosphate pathway. Network analysis revealed that these metabolic changes were associated with membrane raft reorganization and receptor-mediated signaling involving epidermal growth factor receptor and G-protein subunits. Additional effects were observed in pathways related to chromatin organization and post-translational regulation.

THz radiation induces coordinated remodeling of metabolic and regulatory networks in melanoma cells without cytotoxicity. These findings highlight the role of membrane-associated signaling in mediating THz-induced cellular responses and provide insight into potential biomedical applications of THz technologies.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is an independent risk factor for cardiovascular disease (CVD). While gut bacteria have been linked to CVD, the role of intestinal fungi in subclinical coronary atherosclerosis (SCA) remains unclear. In this study, we aimed to investigate the association between the gut mycobiome and SCA in MASLD.

A cross-sectional study was conducted among 103 MASLD patients without established CVD. Fibrosis and steatosis were assessed using magnetic resonance elastography (MRE) and proton density fat fraction, respectively. SCA was defined by coronary artery calcification (CAC). Fecal fungal composition was analyzed via internal transcribed spacer sequencing.

Mean age was 60.8 ± 11.2 years; 51.5% were men; 20.4% had cirrhosis. CAC correlated with MRE (r = 0.489, p < 0.001), interleukin-6 (r = 0.407, p < 0.001), and tumor necrosis factor-α (r = 0.254, p = 0.018), but not proton density fat fraction. Cirrhosis patients had higher CAC than F0–F3 (456.9 vs. 205.9, p = 0.033). Candida albicans (C. albicans) abundance was greater in cirrhosis and correlated with CAC (r = 0.403, p < 0.001) and MRE (r = 0.212, p = 0.032). In multivariate analysis, older age, diabetes, obesity, cirrhosis, and enriched C. albicans independently predicted CAC ≥ 100 AU in MASLD.

In MASLD, cirrhosis and C. albicans enrichment are independently associated with higher SCA burden, suggesting advanced liver disease and a potential fungal contribution to CVD pathogenesis.

To observe the clinical efficacy of Jiawei Lizhong Tang combined with dorsal Yu acupoint embedding in patients with non-alcoholic steatohepatitis (NASH).

A total of 118 patients with NASH who attended the Department of Gastroenterology at Liuzhou Hospital of Traditional Chinese Medicine from January 2020 to December 2022 were selected as study subjects. The participants were randomly assigned to either the control group or the observation group using a random number table, with 59 cases in each group. The control group received treatment with Western medicine (compound glycyrrhizin capsule), whereas the observation group received treatment with traditional Chinese medicine combined with thread embedding (Jiawei Lizhong Tang combined with dorsal Yu acupoints embedding). Both groups received a treatment course of 12 weeks. The following anthropometric indicators were measured: weight, waist circumference, and body mass index. Liver function was assessed by measuring alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and total bilirubin (TBIL). Lipid profile indicators included triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). Blood glucose indicators included fasting blood glucose, fasting insulin (FINS), and insulin resistance index (HOMA-IR). Additionally, liver stiffness measurement (LSM), controlled attenuation parameter (CAP), and liver/spleen CT ratio were assessed. Clinical efficacy was evaluated at the end of the treatment period.

After 12 weeks of treatment, significant improvements were observed in weight, waist circumference, BMI, serum ALT, AST, GGT, TBil, TG, TC, LDL-C, HDL-C, fasting glucose, FINS, HOMA-IR, LSM, CAP, and liver/spleen CT ratio in both groups compared to baseline (P＜0.05). The improvements in these indicators were significantly better in the observation group than in the control group after treatment (P＜0.05).

The treatment of NASH with Jiawei Lizhong Tang combined with dorsal Yu acupoint embedding effectively improves patient condition, reduces liver function damage, regulates blood lipids, insulin resistance, and hepatic steatosis. The therapeutic effect is superior to that of Western medicine therapy.

Insulin resistance is a common extrahepatic manifestation of hepatitis C virus (HCV) infection (HCVi), but its mechanism is poorly understood. While systemic insulin resistance is documented, portal insulin dynamics, a key regulator of hepatic metabolism, remain unexplored. This study aimed to investigate the relationship between insulin, the gut-liver axis, and immunometabolic changes in patients with HCV.

HCV patients were evaluated before (HCVi; n = 29) and after sustained virologic response (SVR) achieved with sofosbuvir/velpatasvir treatment (SVR, n = 23) (NCT02400216). Liver biopsies, portal blood, and peripheral blood were collected at both phases. Statistical analyses were conducted using Wilcoxon rank-sum tests, Mann-Whitney tests, and Pearson’s correlation coefficients to assess differences and associations across insulin, glucose, cytokines, metabolites, immune cells, and hepatic liver transcriptomics to elucidate impaired insulin homeostasis in HCVi.

HCV patients had significantly reduced portal insulin compared to SVR (p = 0.02), while peripheral insulin, portal glucose, and peripheral glucose remained unchanged. Portal insulin correlated positively with proinflammatory cytokines and vascular injury markers and negatively with CD8/CD62L/CD45RA/CD3 cells (naive cytotoxic T-cells) and non-standard nucleotides. Hepatic transcriptomic analysis revealed portal insulin correlated positively with immune and negatively with amino acid pathways, reflecting insulin’s role in the perturbations of immunometabolism during HCVi.

Lower portal insulin during HCVi is associated with changes consistent with altered pancreatic insulin secretion and decreased hepatic insulin extraction. The observed correlations support a potential relationship between the immune response and insulin dynamics, indicating an interplay between the immune system, metabolism, and insulin in HCVi, with clinical implications for the management of dysglycemia.