Böttinger Erwin P
Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.
Semin Nephrol. 2007 May;27(3):309-20. doi: 10.1016/j.semnephrol.2007.02.009.
Chronic progressive kidney diseases typically are characterized by loss of differentiated epithelial cells and activation of mesenchymal cell populations leading to renal fibrosis in response to a broad range of diverse renal injuries. Recent evidence has indicated that epithelial microinjury leads to unbalanced epithelial-mesenchymal communication to initiate the fibrotic response. Transforming growth factors beta constitute a large family of cytokines that control key cellular responses in development and tissue repair. Activation of autocrine and paracrine transforming growth factor-beta signaling cascades in the context of epithelial microinjuries initiate a variety of cell type-dependent signaling and activity profiles, including epithelial apoptosis and epithelial-to-mesenchymal transition, that trigger fibrogenic foci and initiate progressive fibrogenesis in chronic renal injury.
慢性进行性肾病通常的特征是分化的上皮细胞丢失以及间充质细胞群活化，从而在多种不同的肾损伤反应中导致肾纤维化。最近的证据表明，上皮微损伤会导致上皮-间充质通信失衡，从而引发纤维化反应。转化生长因子β构成一大类细胞因子，可控制发育和组织修复中的关键细胞反应。在上皮微损伤的情况下，自分泌和旁分泌转化生长因子β信号级联的激活会引发多种细胞类型依赖性的信号传导和活性谱，包括上皮细胞凋亡和上皮-间充质转化，这些会触发纤维化病灶并在慢性肾损伤中引发进行性纤维化。
