Departamento de Fisiología y Farmacología, Universidad de Salamanca, Edificio Departamental, Campus Miguel de Unamuno, Salamanca, Spain.
EMBO Mol Med. 2009 Sep;1(6-7):303-14. doi: 10.1002/emmm.200900043.
Recent advances in our understanding of the molecular pathways that govern the association of inflammation with organ fibrosis and cancer point to the epithelial to mesenchymal transition (EMT) as the common link in the progression of these devastating diseases. The EMT is a crucial process in the development of different tissues in the embryo and its reactivation in the adult may be regarded as a physiological attempt to control inflammatory responses and to 'heal' damaged tissue. However, in pathological contexts such as in tumours or during the development of organ fibrosis, this healing response adopts a sinister nature, steering these diseases towards metastasis and organ failure. Importantly, the chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.
近年来，我们对调控炎症与器官纤维化和癌症关联的分子途径的理解取得了进展，上皮间质转化（EMT）被认为是这些破坏性疾病进展的共同纽带。EMT 是胚胎中不同组织发育的关键过程，其在成人中的重新激活可能被视为控制炎症反应和“修复”受损组织的生理尝试。然而，在肿瘤或器官纤维化的发展等病理情况下，这种修复反应呈现出险恶的性质，使这些疾病向转移和器官衰竭发展。重要的是，纤维化和癌细胞共有的慢性炎症微环境成为诱导病理性 EMT 的决定性因素。
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