Arthur M J, Iredale J P
University Medicine, Southampton General Hospital.
J R Coll Physicians Lond. 1994 May-Jun;28(3):200-8.
In progressive liver fibrosis, the rate [corrected] of extracellular collagen deposition exceeds its rate of degradation. Collagen and related proteins are synthesised in the fat-storing liver cells (lipocytes). When injured, these cells proliferate and change into myofibroblast-like cells, secreting even more collagen into the extracellular space. The degradation of collagen is accomplished by metalloproteinases, whose activity is reduced by tissue inhibitors (TIMPs). Injured lipocytes produce an excess of these inhibitors. The final result of lipocyte injury is thus progressive liver fibrosis. There is evidence that TIMPs also play a role in progressive fibrosis in other tissues.
在进行性肝纤维化过程中,细胞外胶原蛋白沉积速率[校正后]超过其降解速率。胶原蛋白及相关蛋白在贮脂肝细胞(脂肪细胞)中合成。这些细胞受损时会增殖并转变为成肌纤维细胞样细胞,向细胞外间隙分泌更多胶原蛋白。胶原蛋白的降解由金属蛋白酶完成,其活性会被组织抑制剂(TIMPs)降低。受损的脂肪细胞会产生过量的这些抑制剂。因此,脂肪细胞损伤的最终结果是进行性肝纤维化。有证据表明,TIMPs在其他组织的进行性纤维化中也起作用。