Genesis of hepatic fibrosis and its biochemical markers
Genesis of hepatic fibrosis and its biochemical markers
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DOI：
10.1080/00365510701668516
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发表时间：
2008-01-01
影响因子：
2.1
通讯作者：
Vasudevan, D. M.
中科院分区：
文献类型：
--
作者：
Das, S. K.;Vasudevan, D. M.
肝纤维化的特征是细胞外基质（ECM）在肝脏的异常积聚，这是由胶原纤维沉积增加和降解减少引起的。纤维化肝损伤导致肝星状细胞（HSC）活化。替代标记物逐渐被生物标记物所取代，这些生物标记物反映了细胞外基质合成和降解之间的复杂平衡。一旦肝星状细胞被激活，之前的基质发生变化，反复的损伤刺激将使激活状态永久化。ECM指导细胞分化、迁移、增殖和纤维化激活或失活。细胞外基质的代谢受基质金属蛋白酶（MMP）及其特异性组织抑制剂（TIMP）的密切调控。虽然肝活检结合结缔组织染色已成为诊断的主要方法，但仍需要侵入性较小的方法。这些诊断指标应结合肝功能检查、超声检查和临床表现加以考虑。
Liver fibrosis is characterized by an abnormal hepatic accumulation of extracellular matrix (ECM) that results from both increased deposition and reduced degradation of collagen fibres. Fibrotic liver injury results in activation of the hepatic stellate cell (HSC). Surrogate markers are gradually being substituted for biomarkers that reflect the complex balance between synthesis and degradation of the extracellular matrix. Once the hepatic stellate cell is activated, the preceding matrix changes and recurrent injurious stimuli will perpetuate the activated state. The ECM directs cellular differentiation, migration, proliferation and fibrogenic activation or deactivation. The metabolism of the extracellular matrix is closely regulated by matrix metalloproteinases (MMP) and their specific tissue inhibitors (TIMP). Although liver biopsy combined with connective tissue stains has been a mainstay of diagnosis, there is a need for less invasive methods. These diagnostic markers should be considered in combination with liver function tests, ultrasonography and clinical manifestations.