Objective To observe and analyze the relationships among the level of interleukin 25 (IL-25), the stage of liver fibrosis and the polarization of hepatic M2 macrophages in patients with non-alcoholic fatty liver disease (NAFLD). Methods A total of 36 patients with NAFLD and 20 control patients were enrolled. Fibrotouch, HE staining, and immunohistochemistry were used to evaluate the stage of liver fibrosis. Patients with NAFLD were classified into groups of mild liver fibrosis (F1) (20 cases) and significant liver fibrosis (≥ F2) (16 cases). The level of serum IL-25 in each group was detected by ELISA. Real-time fluorescent quantitative PCR was used to detect the hepatic mRNA expression levels of IL-25, collagen1 (Col1), α mooth muscle actin (α-SMA), macrophage mannose receptor 1 (CD206/MR1) and transglutaminase 2 (TGM2). Immunohistochemistry was used to detect the protein levels of IL-25, α-SMA, CD206 and TGM2. Results There was no significant difference in the level of serum IL-25 among groups. Compared with patients in the control group and the mild liver fibrosis group, patients with significant liver fibrosis showed reduced mRNA expression levels of IL-25, CD206, and TGM2 in addition to lower levels of hepatic IL-25 protein and less polarization of M2 macrophages. Conclusion Down-regulation of IL-25 is accompanied by a decrease in the number of the M2 macrophages with the progression of liver fibrosis in NAFLD patients.
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Nat Rev Gastroenterol Hepatol
January 2025
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Ministerio de Sanidad, Madrid, Spain.
Two main stages are differentiated in patients with advanced chronic liver disease (ACLD), one compensated (cACLD) with an excellent prognosis, and the other decompensated (dACLD), defined by the appearance of complications (ascites, variceal bleeding and hepatic encephalopathy) and associated with high mortality. Preventing the progression to dACLD might dramatically improve prognosis and reduce the burden of care associated with ACLD. Portal hypertension is a major driver of the transition from cACLD to dACLD, and a portal pressure of ≥10 mmHg defines clinically significant portal hypertension (CSPH) as the threshold from which decompensating events may occur.
View Article and Find Full Text PDFBackground: Metabolic dysfunction-associated steatotic liver disease (MASLD) includes simple steatosis and metabolic dysfuncion-associated steatohepatitis (MASH), with fibrosis in MASH serving as a critical prognostic marker. This study investigates the effects of Roux-en-Y gastric bypass (RYGB) on fibrotic MASH, assessed using the fibrotic NASH index (FNI) and the non-invasive NASH detection score (NI-NASH-DS), as well as provides further data on the diagnostic accuracy of both scores.
Methods: A retrospective cohort study was conducted involving 104 individuals (91.
Nat Med
January 2025
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH, USA.
No therapy has been shown to reduce the risk of major adverse liver outcomes (MALO) in patients with cirrhosis due to metabolic dysfunction-associated steatohepatitis (MASH). The Surgical Procedures Eliminate Compensated Cirrhosis In Advancing Long-term (SPECCIAL) observational study compared the effects of metabolic surgery and nonsurgical treatment in patients with obesity and compensated histologically proven MASH-related cirrhosis. Using a doubly robust estimation methodology to balance key baseline characteristics between groups, the time-to-incident MALO was compared between 62 patients (68% female) who underwent metabolic surgery and 106 nonsurgical controls (71% female), with a mean follow-up of 10.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Zhuhai Institute of Translational Medicine, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Jinan University, Zhuhai 519000, China; State Key Laboratory of Bioactive Molecules and Druggability Assessment, The Biomedical Translational Research Institute, Health Science Center (School of Medicine), Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China. Electronic address:
Previous studies have established that γδ T cells play a significant role in liver fibrosis. However, their specific functions and mechanisms in fibrotic liver tissue remain unclear. Using online microarray expression profiles, we observed that USF3 was upregulated in patients with liver fibrosis and was associated with immune cells.
View Article and Find Full Text PDFActa Pharmacol Sin
January 2025
Department of Medical Microbiology & Parasitology, MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Metabolic dysfunction-associated steatotic liver disease (MASLD) covers a broad spectrum of profile from simple fatty liver, evolving to metabolic dysfunction-associated steatohepatitis (MASH), to hepatic fibrosis, further progressing to cirrhosis and hepatocellular carcinoma (HCC). MASLD has become a prevalent disease with 25% in average over the world. MASH is an active stage, and requires pharmacological intervention when there is necroptotic damage with fibrotic progression.
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