Hepatic fibrosis is not only a pathological process of hepatic self-repair after chronic liver injury， but also a critical stage in the progression of chronic liver disease to liver cirrhosis. Studies have shown that as a pro-inflammatory form of programmed cell death， pyroptosis plays an important role in various diseases and is also considered a potential therapeutic target for hepatic fibrosis. This article systematically reviews the association of pyroptosis in hepatocytes， hepatic stellate cells， and hepatic macrophages with hepatic fibrosis and discusses pyroptosis-mediated therapeutic strategies targeting hepatic fibrosis.

Primary biliary cholangitis （PBC） is a cholestatic autoimmune liver disease characterized by the injury of small intrahepatic bile ducts， and at present， the pathogenesis of PBC remains unclear. Recent studies have shown that bile acid metabolism disorder and gut microbiota imbalance play a key role in the development and progression of PBC， and they form a complex and dynamic interaction network via the “gut-liver axis” and regulate core physiopathological processes such as immune response， metabolic homeostasis， and inflammatory response in a synergistic manner. This article systematically elaborates on the abnormal features of bile acid metabolism and gut microbiota in PBC， discusses their synergistic mechanisms in PBC， and then proposes a combined strategy of targeting bile acid receptors and modulating gut microbiota， in order to overcome the limitations of current treatment modalities and provide new insights and directions for the clinical management of PBC.

Depression is a chronic brain dysfunctional disease mainly due tomood disorders.Currently,the pathogenesis of depression is unclear,and its pathogenesis,pathophysiology and treatment have consistently been a major focus of academic research.This review provides an overview of the role of serum inflammatory factors in the pathogenesis,diagnosis,and treatment of depression.The inflammatory factor pathway provides a theoretical basis for the development of diagnostic and therapeutic methods for depression.It is expected to provide accurate personalized treatment for patients with depression through the treatment of inflammatory factors,improve the treatment outcomest,and reduce the risk of disease progression.

Depression is a chronic brain dysfunctional disease mainly due tomood disorders.Currently,the pathogenesis of depression is unclear,and its pathogenesis,pathophysiology and treatment have consistently been a major focus of academic research.This review provides an overview of the role of serum inflammatory factors in the pathogenesis,diagnosis,and treatment of depression.The inflammatory factor pathway provides a theoretical basis for the development of diagnostic and therapeutic methods for depression.It is expected to provide accurate personalized treatment for patients with depression through the treatment of inflammatory factors,improve the treatment outcomest,and reduce the risk of disease progression.

Primary biliary cholangitis(PBC)is a persistent inflammatory autoimmune liver disease characterized by inflammatory injury and cholestasis in the small intrahepatic bile ducts.At present,the exact pathogenesis of PBC remains unknown,but a consensus has been reached on the fact that PBC is the result of the synergistic effect of various factors.In the cascade of immune and inflammatory reactions associated with PBC,macrophages appear as essential immune cells and actively participate in the damage to bile duct epithelial cells.This article introduces the origin and heterogeneity of macrophages in PBC and reviews the potential role of macrophages in the pathogenesis of PBC.

Primary biliary cholangitis （PBC） is a chronic autoimmune disease of cholestasis in which immune factors lead to progressive small bile duct destruction， cholestasis， and eventually liver fibrosis， liver cirrhosis， and even liver failure. Macrophages， as a group with functional heterogeneity， play different roles in the whole disease process of PBC. This article summarizes the possible ways by which macrophages are involved in the pathogenesis of PBC and discusses their impact on the disease and the potential therapeutic targets of macrophages. It is pointed out that macrophages are mainly involved in innate immunity in PBC injury and are associated with gut microbiota dysbiosis， and they are also associated with cholestasis， liver fibrosis， and liver cirrhosis in the later stages of the disease.

Primary biliary cholangitis （PBC） is a liver autoimmune disease with a strong genetic tendency characterized by the degeneration and necrosis of bile duct epithelial cells， and it is often observed in middle-aged and elderly women. With the continuous development of genome-wide association studies， the genetic susceptibility of PBC has attracted more and more attention. This article elaborates on the research advances in the genetic susceptibility genes closely associated with PBC， in order to provide effective targets for the treatment of PBC.

Primary biliary cholangitis (PBC) is a cholestatic autoimmune liver disease characterized by a high incidence rate in middle-aged and elderly women, lymphocyte infiltration in small bile ducts, and cholestasis. Main clinical manifestations include fatigue and pruritus caused by cholestasis. Ursodeoxycholic acid and obeticholic acid are currently approved therapeutic drugs for PBC and exert a therapeutic effect by regulating bile acid metabolism and specifically and effectively improving cholestasis. This article introduces the physiological and pathological changes of bile acids in disease states and summarizes the possible ways in which bile acid metabolism is involved in the pathogenesis of diseases and the current treatment methods for bile acid metabolism. It is pointed out that the changes of bile acid metabolism in PBC are mainly associated with anion exchanger 2 deficiency, innate genetic variation and acquired adaptive changes of bile acid metabolism transporters and nuclear receptors, and changes in the structure of intestinal flora.

Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease, and may progress to cirrhosis and associated with complications of end-stage liver disease. The immunological characteristic of PBC is the presence of anti-mitochondrial autoantibodies (AMAs), and some anti-nuclear antibodies (ANAs) have high specificity for the diagnosis of PBC. In recent years, it has been found that anti-gp210, anti-sp100 and anti-centromere antibodies are correlated with the severity of PBC, treatment response to ursodeoxycholic acid (UDCA) and poor prognosis. However, correlation between AMAs and disease progression of PBC is still in controversial. This article reviewed the progress in research on the influence of autoantibodies on biochemical response and prognosis of PBC.

Objective To investigate the correlation between ADAM33 T1, S2 gene polymorphism and Bronchial asthma risk in china. Methods We retrived the relevant published studies about ADAM33 T1, S2 gene polymorphism and bronchial asthma risk. Then we divided the population into Chinese and other Asian population. Odds ratio (OR) of Case group and control group was selected as the effect index. Stata 11.0 software was used to calculate heterogeneity test, ORs and 95%CI of two areas, and gave the forest plot and funnel plot of meta results. Results A total of 27 studies were included in this analysis,18 studies in ADAM33 T1 site were 3881 cases in case group, and 3780 cases in control group;and 14 studies in ADAM33 S2 site were 3222 cases in case group, and 3513 cases in control group. Additive model, dominant model, recessive model of ADAM33 T1 in Chinese had association with the susceptibility of bronchial asthma. The results were OR=1.488, 95% CI:1.002-2.167 in Additive model, OR=1.619, 95%CI:1.059-2.475 in dominant model;OR=2.523, 95%CI:1.910-3.333 in recessive model. Three models of ADAM33 T1 in other Asian country had no association with the susceptibility of Bronchial Asthma. Three gene model of ADAM33 S2 in Asian had no association with bronchial asthma susceptibility. Except ADAM33 T1 polymorphism in recessive model, other mode of T1, S2 had no publication bias in Chinese population. Conclusion There are association between ADAM33 T1 gene polymorphism and bronchial asthma, but ADAM33 S2 gene polymorphism and bronchial asthma have no association in Chinese population.