Organ fibrosis is a process in which cellular homeostasis is disrupted and extracellular matrix is excessively deposited. Fibrosis can lead to vital organ failure and there are no effective treatments yet. Although epithelial-mesenchymal transition (EMT) may be one of the key cellular mechanisms, the underlying mechanisms of fibrosis remain largely unknown. EMT is a cell phenotypic process in which epithelial cells lose their cell-to-cell adhesion and polarization, after which they acquire mesenchymal features such as infiltration and migration ability. Upon injurious stimulation in different organs, EMT can be triggered by multiple signaling pathways and is also regulated by epigenetic mechanisms. This narrative review summarizes the current understanding of the underlying mechanisms of EMT in fibrogenesis and discusses potential strategies for attenuating EMT to prevent and/or inhibit fibrosis. Despite better understanding the role of EMT in fibrosis development, targeting EMT and beyond in developing therapeutics to tackle fibrosis is challenging but likely feasible.

中文翻译：

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器官纤维化发展中的上皮-间质转化：当前的理解和治疗策略。

器官纤维化是细胞稳态被破坏和细胞外基质过度沉积的过程。纤维化可导致重要器官衰竭，目前还没有有效的治疗方法。尽管上皮间质转化 (EMT) 可能是关键的细胞机制之一，但纤维化的潜在机制仍然很大程度上未知。EMT是一种细胞表型过程，其中上皮细胞失去其细胞间的粘附和极化，之后它们获得间充质特征，例如浸润和迁移能力。在不同器官受到伤害性刺激后，EMT 可以由多种信号通路触发，也受表观遗传机制的调节。这篇叙述性综述总结了目前对 EMT 在纤维化中的潜在机制的理解，并讨论了减弱 EMT 以预防和/或抑制纤维化的潜在策略。尽管更好地了解 EMT 在纤维化发展中的作用，但在开发治疗纤维化的治疗方法中靶向 EMT 及其他方面具有挑战性，但可能是可行的。