Organ Fibrosis and Autoimmunity: The Role of Inflammation in TGFβ-Dependent EMT

Recent advances in our understanding of the molecular pathways that control the link of inflammation with organ fibrosis and autoimmune diseases point to the epithelial to mesenchymal transition (EMT) as the common association in the progression of these diseases characterized by an intense inflammatory response. EMT, a process in which epithelial cells are gradually transformed to mesenchymal cells, is a major contributor to the pathogenesis of fibrosis. Importantly, the chronic inflammatory microenvironment has emerged as a decisive factor in the induction of pathological EMT. Transforming growth factor-beta (TGF-beta), a multifunctional cytokine, plays a crucial role in the induction of fibrosis, often associated with chronic phases of inflammatory diseases, contributing to marked fibrotic changes that severely impair normal tissue architecture and function. The understanding of molecular mechanisms underlying EMT-dependent fibrosis has both a basic and a translational relevance, since it may be useful to design therapies aimed at counteracting organ deterioration and failure. To this end, we reviewed the recent literature to better elucidate the molecular response to inflammatory/fibrogenic signals in autoimmune diseases in order to further the specific regulation of EMT-dependent fibrosis in more targeted therapies.

Automated summary

Recent advances in understanding the molecular pathways linking inflammation with organ fibrosis and autoimmune diseases have identified EMT as a common association. The chronic inflammatory microenvironment plays a crucial role in inducing pathological EMT, with TGF-beta being a key player in fibrosis induction. Further research aims to target EMT-dependent fibrosis in autoimmune diseases through a better understanding of molecular responses to inflammatory signals.