Kovacs E J, DiPietro L A
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Stritch School of Medicine, Maywood, Illinois 60153.
FASEB J. 1994 Aug;8(11):854-61. doi: 10.1096/fasebj.8.11.7520879.
The pathogenesis of fibrotic disorders is similar regardless of the tissues involved. Inflammatory leukocytes infiltrate the site triggered by chemotactic and activating mediators. This is followed by the elaboration of cytokines that directly and indirectly induce the proliferation of fibroblasts and endothelial cells and the deposition of extracellular matrix (ECM). In the absence of inhibitory signals, the continued production of these mediators sustains the connective tissue accumulation, which results in permanent alteration in tissue structure and function.
无论涉及何种组织，纤维化疾病的发病机制都是相似的。炎症白细胞在趋化和激活介质触发的部位浸润。随后会产生细胞因子，这些细胞因子直接或间接诱导成纤维细胞和内皮细胞增殖以及细胞外基质（ECM）沉积。在缺乏抑制信号的情况下，这些介质的持续产生维持结缔组织的积累，从而导致组织结构和功能的永久性改变。
