Kissin Eugene, Korn Joseph H
Boston University School of Medicine, 71 East Concord Street, Boston, MA 02118, USA.
Curr Rheumatol Rep. 2002 Apr;4(2):129-35. doi: 10.1007/s11926-002-0008-y.
Tissue fibrosis is the result of a complex series of events focusing on regulation of fibroblast proliferation, synthesis of extracellular matrix, and apoptosis. Transforming growth factor-beta is important for the stimulation of the fibrotic response by promoting the production of extracellular matrix proteins, by promoting the differentiation of the myofibroblast cell morphology, and by protecting these cells against apoptotic stimuli. Other cytokines such as interleukin-1 may have stimulatory and counter-regulatory effects on fibrosis. The effects of these signaling molecules depend on cellular environment and are organ specific. Furthermore, intercellular interactions and cell-matrix interactions can stimulate or inhibit the apoptotic pathway. Through selective inhibition of apoptosis in myofibroblasts, fibrosis can become dysregulated and lead to diseases such as systemic sclerosis.
组织纤维化是一系列复杂事件的结果，这些事件主要围绕成纤维细胞增殖的调节、细胞外基质的合成以及细胞凋亡展开。转化生长因子-β通过促进细胞外基质蛋白的产生、促进肌成纤维细胞形态的分化以及保护这些细胞免受凋亡刺激，在刺激纤维化反应中起着重要作用。其他细胞因子如白细胞介素-1可能对纤维化具有刺激和反调节作用。这些信号分子的作用取决于细胞环境，并且具有器官特异性。此外，细胞间相互作用和细胞-基质相互作用可以刺激或抑制凋亡途径。通过选择性抑制肌成纤维细胞的凋亡，纤维化可能会失调并导致诸如系统性硬化症等疾病。
