HSC凋亡与肝纤维化逆转的研究进展

肝星状细胞(HSC)在肝纤维化形成中起核心作用,其凋亡是肝纤维化逆转的主要机制之一.深入研究HSC凋亡的调控机理及HSC凋亡在肝纤维化逆转中的作用,对肝纤维化的防治具有重要意义.     

肝星状细胞及相关细胞因子在肝纤维化形成中的作用

肝纤维化(hepatic fibrosis)是指肝脏内弥漫性细胞外基质(extracellular matrix,ECM)过度沉积的病理过程.肝星状细胞(hepatic stellate cells,HSC)被认为是ECM的主要来源细胞,在肝纤维化发生发展中起着关键作用.另外,各种病因引起肝细胞损伤时,Kupffers细胞(KF),肝窦内皮细胞等分泌一系列细胞因子,通过旁分泌和自分泌方式作用于邻近的HSC,影响其增殖,趋化和ECM代谢.因此,HSC及细胞因子与肝纤维化的发生发展关系极为密切,阐明其关系,有助于以HSC为靶点的肝纤维化方面的研究,现就其关系分别综述如下.     

活性氧簇与肝纤维化发病的研究进展

肝星状细胞(HSC)的激活是肝纤维化发病的中心事件,而活性氧簇(ROS)是肝纤维化发病的重要介质.不同来源的ROS在HSC激活的各个阶段所起的作用不同,它参与了肝纤维化发病的全过程.     

肝星状细胞与肝纤维化

肝纤维化是各种慢性肝病共有的病理改变,逆转肝纤维化可阻止大多数慢性肝病进展。肝星状细胞(HSC)是肝内一种具有多功能、变化不定的非实质细胞,HSC活化是肝纤维化发生的中心环节。阐明其关系,有助于以HSC为靶点的肝纤维化方面的研究。     

肝星状细胞与肝纤维化的恢复

各种病因的肝脏损伤都伴有肝星状细胞（HSC）的活化.活化HSC分泌大量的细胞外基质导致肝纤维化.探讨HSC的改变在肝纤维化恢复中的作用,将为肝纤维化的治疗提供方向.     

肝组织特异性基因启动子靶向干预肝纤维化的研究现状

肝纤维化(LF)是各种慢性肝病进展为肝硬化的必经阶段,而肝星状细胞(HSC)的活化是肝纤维化发生发展的中心环节.近年来,随着肝纤维化分子机制研究不断深入,针对HSC的基因调控成为治疗肝纤维化的新策略.但如何使干预措施靶向作用到HSC而不影响肝内其他细胞,仍是基因治疗领域的一大挑战.利用肝组织特异性基因启动子构建载体可在...     

肝星状细胞与炎症的关系

肝星状细胞(hepatic stellate cell,HSC)与肝纤维化形成密切相关,使得HSC被广泛地关注,肝纤维化是慢性肝病共有的病理改变,是肝脏对慢性损伤的一种修复反应,其特征为细胞外基质(extracellular matrix,EMC)的过度表达和异常沉积。活化的HSC是肝纤维化发生中EMC的主要来源,是肝纤     

TGFβ1信号与肝纤维化

肝星状细胞(HSC)是肝纤维化发生的关键细胞,转化生长因子β1(TGFβ1)是活化HSC、促进细胞外基质(ECM)分泌的重要细胞因子,其在肝纤维化的发生发展中有重要的调节作用,文章通过TGFβ1信号转导对HSC的作用来阐述TGFβ1信号与肝纤维化的关系.     

肝纤维化中肝星状细胞内主要信号转导通路

肝纤维化是肝脏对各种慢性刺激进行损伤修复反应时,以胶原为主的细胞外基质(ECM)在肝内大量沉积的病理过程.活化的肝星状细胞(HSC)是肝纤维化时产生ECM的主要细胞.细胞因子、氧化应激以及ECM的改变等外部因素通过一定的细胞内信号转导通路激活HSC.了解HSC活化的信号转导通路能从根本上为治疗肝纤维化提供更多更有效的思路和方法.目前研究较多的信号途径有TGF-β/Smad通路、MAPK通路、PI3K通路、JAK/STAT通路、NF-κB通路、过氧化物酶体增殖物激活受体通路等.本文简要综述了肝纤维化时HSC中主要的细胞内信号转导通路.     

肝星状细胞在血吸虫病肝纤维化形成及调控中的作用

肝星状细胞(hepatic stellate cell,HSC)是肝脏组织的一种间质细胞,具有多种生理功能,对肝纤维化的形成与转归起到关键作用.HSC同样在血吸虫病肝纤维化形成及其调节中起到重要作用.该文就HSC的生物学特性、活化及其在血吸虫病肝纤维化中的作用作一综述.     

State of knowledge of helminth fauna of freshwater fishes of Poland

A total 89 fish and lamprey species has been recorded from Polish freshwater habitats. Twenty-seven of them (30.3%) have not been surveyed for parasitic helminthes. Some of the latter fishes are either rare or not easily accessible. Other live only in specific habitats in scattered localities. An important obstacle for studying parasite faunas of some fishes may be their status on an endangered species. Among the non-surveyed fishes, are those which have been relatively recently introduced to Poland or migrated there on their own. The present paper attempts to review all hitherto not studied helminthologically fish species, their habitats, localities and current protection status.     

高血压降压治疗目标的再认识

根据传统的高血压水平的定义,1993年WHO高血压治疗指南提出血压控制目标为<140/90mm Hg(1mm Hg=0.133kPa),但是并非所有患者都必须将血压降至同一水平,而应根据患者情况进行个体化治疗。Framingham进行的一项长达10～12年的心血管事件研究发现,第5年后,正常上限血压[收缩压(SBP     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.