Stratified analysis of the correlation between wedged hepatic venous pressure and portal venous pressure in patients with portal hypertension.

To evaluate the differences in the agreement between wedged hepatic venous pressure (WHVP) and portal venous pressure (PVP) at different hepatic venous pressure gradient (HVPG) levels to identify specific HVPG thresholds where WHVP can reliably estimate PVP, thus enhancing the accuracy of risk stratification and treatment decision-making for portal hypertension (PHT) patients. A multicenter study of 616 patients with PHT from three centers was stratified into five groups by their HVPG: HVPG < 12 (group A), 12 ≤ HVPG < 16 mmHg (group B), 16 ≤ HVPG < 20 mmHg (group C), 20 ≤ HVPG < 24 mmHg (group D), HVPG ≥ 24 mmHg (group E). Concordance was analyzed using Pearson's correlation coefficient (R), the intraclass correlation coefficient (ICC), and Bland‒Altman analysis in each HVPG stratum.

Alterations in the gut microbiome after transjugular intrahepatic portosystemic shunt in patients with hepatitis B virus-related portal hypertension.

Background: Gut microbiota (GM) affects the progression and response to treatment in liver diseases. The GM composition is diverse and associated with different etiologies of liver diseases. Notably, alterations in GM alterations are observed in patients with portal hypertension (PH) secondary to cirrhosis, with hepatitis B virus (HBV) infection being a major cause of cirrhosis in China.

Procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 promotes collagen cross-linking and ECM stiffening to induce liver fibrosis.

Procollagen-lysine 2-oxoglutarate 5-dioxygenase 2 (Plod2) is a key collagen lysyl hydroxylase mediating the formation of collagen fiber and stabilized collagen cross-links, and has been identified in several forms of fibrosis. However, the potential role and regulatory mechanism of Plod2 in liver fibrosis remain unclear yet. Mouse liver fibrosis models were induced by injecting carbon tetrachloride (CCl) intraperitoneally.

Correlation between hepatic venous pressure gradient and portal pressure gradient in patients with autoimmune cirrhotic portal hypertension and collateral branches of the hepatic vein.

Aim: To assess the correlation and agreement between hepatic venous pressure gradient (HVPG) and portal pressure gradient (PPG) in patients with autoimmune liver diseases (ALD) and portal hypertension, and to investigate the extent to which hepatic vein collateralization affects the accuracy of this assessment.

Methods: Ninety-eight patients with ALD between 2017 and 2021 who underwent transjugular intrahepatic portosystemic shunt with conventional and innovative 15 mL pressurized contrast were selected to measure wedged hepatic venous pressure (WHVP) and portal venous pressure and to calculate the HVPG and PPG. Pearson's correlation was used for correlation analysis between the two groups.

Neuron-Glial Antigen 2 Participates in Liver Fibrosis via Regulating the Differentiation of Bone Marrow Mesenchymal Stem Cell to Myofibroblast.

Neuron-glial antigen 2 (NG2, gene name: ) has been characterized as an important factor in many diseases. However, the pathophysiological relevance of NG2 in liver disease specifically regarding bone marrow mesenchymal stem cell (BMSC) differentiation to myofibroblast (MF) and the molecular details remain unknown. Human liver tissues were obtained from patients with different chronic liver diseases, and mouse liver injury models were induced by feeding a methionine-choline-deficient and high-fat diet, carbon tetrachloride administration, or bile duct ligation operation.

Circ_0007534 as new emerging target in cancer: Biological functions and molecular interactions.

Circular RNA (circRNAs), an important member of the non-coding RNA (ncRNA) family, are widely expressed in a variety of biological cells. Owing to their stable structures, sequence conservations, and cell- or tissue-specific expressions, these RNA have become a popular subject of scientific research. With the development of sequencing methods, it has been revealed that circRNAs exert their biological function by sponging microRNAs (miRNAs), regulating transcription, or binding to proteins.

Correlation of pressure gradient in three hepatic veins with portal pressure gradient.

Background: The liver is one of the most important organs in the human body, with functions such as detoxification, digestion, and blood coagulation. In terms of vascular anatomy, the liver is divided into the left and the right liver by the main portal vein, and there are three hepatic efferent veins (right, middle, and left) and two portal branches. Patients with impaired liver function have increased intrahepatic vascular resistance and splanchnic vasodilation, which may lead to an increase in the portal pressure gradient (PPG) and cause portal hypertension (PHT).

Silencing IQGAP1 alleviates hepatic fibrogenesis via blocking bone marrow mesenchymal stromal cell recruitment to fibrotic liver.

IQ motif-containing guanosine triphosphatase (GTPase)-activating protein 1 (IQGAP1) is a cytosolic scaffolding protein involved in cell migration. Our previous studies suggest sphingosine 1-phosphate (S1P) triggers bone marrow (BM) mesenchymal stromal cells (BMSCs) to damaged liver, thereby promoting liver fibrosis. However, the role of IQGAP1 in S1P-induced BMSC migration and liver fibrogenesis remains unclear.

Dual Targeting of Angipoietin-1 and von Willebrand Factor by microRNA-671-5p Attenuates Liver Angiogenesis and Fibrosis.

Angipoietin-1 (Angpt1) and von Willebrand factor (VWF) are two important angiogenic molecules that can drive pathologic angiogenesis and progression of liver fibrosis in our previous study. MicroRNAs (miRs) participate in a variety of physiological and pathological processes, including angiogenesis. However, the critical miRs targeting Angpt1 or VWF and potential molecular mechanism underlying liver fibrosis-associated angiogenesis is not clear yet.

Neutrophil recruitment mediated by sphingosine 1-phosphate (S1P)/S1P receptors during chronic liver injury.

Excessive neutrophils are recruited to damaged tissue and cause collateral injury under chronic inflammatory conditions. Sphingosine 1-phosphate (S1P) modulates kinds of physiological and pathological actions by inducing recruitment of various cell types through S1P receptors (S1PRs). This study aimed to detect the S1P/S1PRs-mediated effects on neutrophil recruitment during chronic liver inflammation.

Macrophage Sphingosine 1-Phosphate Receptor 2 Blockade Attenuates Liver Inflammation and Fibrogenesis Triggered by NLRP3 Inflammasome.

NLR family pyrin domain containing 3 (NLRP3) inflammasome accompanies chronic liver injury and is a critical mediator of inflammation-driven liver fibrosis. Sphingosine 1-phosphate (S1P)/S1P Receptor (S1PR) signaling participates in liver fibrogenesis by affecting bone marrow (BM)-derived monocytes/macrophage (BMM) activation. However, the relationship between S1P/S1PR signaling and NLRP3 inflammasome in BMMs remains unclear.

Cannabinoid Receptor 1/miR-30b-5p Axis Governs Macrophage NLRP3 Expression and Inflammasome Activation in Liver Inflammatory Disease.

Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) has been regarded as an important initiator or promoter in multiple inflammatory diseases. However, the relationship between cannabinoid receptor 1 (CB1) and macrophage NLRP3 inflammasome and the corresponding molecular mechanism in liver inflammation remain unclear. Mouse liver injury models were induced by carbon tetrachloride (CCl) or methionine-choline-deficient and high fat (MCDHF) diet.

Gadolinium Chloride Restores the Function of the Gap Junctional Intercellular Communication between Hepatocytes in a Liver Injury.

Background: Gadolinium chloride (GdCl) has been reported to attenuate liver injury caused by a variety of toxicants. Gap junctional intercellular communication (GJIC) is thought to be essential in controlling liver homeostasis and pathology. Here we evaluate the effects of GdCl on functional GJIC and connexin expression in mouse models and primary hepatocytes.

MicroRNA-26b-5p Inhibits Mouse Liver Fibrogenesis and Angiogenesis by Targeting PDGF Receptor-Beta.

Here microRNAs (miRNAs) with potentially therapeutic effects were screened and explored during liver fibrogenesis and angiogenesis via targeting the important mediators. Chimera mice with EGFP bone marrow mesenchymal stromal cells (BMSCs) were fed with methionine-choline-deficient and high-fat (MCDHF) diet to induce liver injury. Increased expression of platelet-derived growth factor receptor-beta (PDGFR-β) was detected in MCDHF mice, with a positive correlation to fibrosis and angiogenesis markers.

The class D scavenger receptor CD68 contributes to mouse chronic liver injury.

Scavenger receptors, which are expressed on monocyte/macrophages, play a central role in many pathogenic processes. Here, we examined the role of the class D scavenger receptor (CD68) in bone marrow-derived monocyte/macrophages (BMMs) in chronic liver injury. The expression pattern of multiple scavenger receptors in two liver injury models (methionine-choline-deficient and high fat (MCDHF), carbon tetrachloride (CCl)) were analyzed by qRT-PCR.