TGF-beta in renal injury and disease.

TGF-beta in renal injury and disease.
复制标题

DOI:
--
复制
发表时间:
2007
影响因子:
3.3
通讯作者:
E. Böttinger
E. Böttinger
中科院分区:
医学2区
文献类型:
--
作者:
E. Böttinger

文献摘要

被引文献

相似文献

慢性进行性肾脏疾病的典型特征在于响应于广泛的不同肾损伤而导致肾纤维化的分化上皮细胞的损失和间充质细胞群的活化。最近的证据表明,上皮微损伤导致不平衡的上皮间质通讯启动纤维化反应。转化生长因子β构成细胞因子的大家族,其控制发育和组织修复中的关键细胞反应。在上皮微损伤的背景下,自分泌和旁分泌转化生长因子-β信号级联的激活启动了多种细胞类型依赖性信号和活性谱,包括上皮细胞凋亡和上皮-间质转化,其触发纤维化灶并启动慢性肾损伤中的进行性纤维化。
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.