Epithelial-mesenchymal transition: An emerging target in tissue fibrosis

Abstract

Epithelial-mesenchymal transition (EMT) is involved in a variety of tissue fibroses. Fibroblasts/myofibroblasts derived from epithelial cells contribute to the excessive accumulation of fibrous connective tissue in damaged tissue, which can lead to permanent scarring or organ malfunction. Therefore, EMT-related fibrosis cannot be neglected. This review highlights the findings that demonstrate the EMT to be a direct contributor to the fibroblast/myofibroblast population in the development of tissue fibrosis and helps to elucidate EMT-related anti-fibrotic strategies, which may enable the development of therapeutic interventions to suppress EMT and potentially reverse organ fibrosis.

miR‐200b‐containing microvesicles attenuate experimental colitis associated intestinal fibrosis by inhibiting epithelial‐mesenchymal transition

“…Fibrosis is usually the final pathological state of many chronic inflammatory diseases and may lead to organ dysfunction . Recently, growing evidence suggests that EMT is a direct contributor to the fibroblast/myofibroblast pool during fibrogenesis . EMT can be induced by the joint action of cytokines, inflammation, reactive oxygen species, and many other factors.…”

The Role of Nrf2 in the Response to Normal Tissue Radiation Injury

“…At a molecular level it has been shown that Nrf2 can form a nuclear complex with nuclear pSmad3 at CAGA sites located in the proximal promoters of TGF-β target genes (79), suppressing gene expression (79, 83). Thus, loss of Nrf2 promotes TGF-β/RSmad signaling, a key factor for promoting epithelial-mesenchymal transitions (84). Conversely, TGF-β/RSmad signaling has been shown to suppress Nrf2-dependent gene expression.…”

Silencing of c-Ski augments TGF-b1-induced epithelial-mesenchymal transition in cardiomyocyte H9C2 cells

“…This study found that the ability of cell migration was increased within a short time (≤ 24 h) after c-Ski knockdown, suggesting that H9C2 cells may express some skeletal proteins or turn to fibroblasts after c-Ski silencing. Previous studies have demonstrated that TGF-b, as the best characterized fibrogenic growth factor [21], is markedly and consistently activated in experimental models of cardiac fibrosis [22] and in fibrotic human hearts [23] For nearly a decade, much research showed that EMT is involved in a variety of tissue fibrosis and is a direct contributor to the fibroblast/ /myofibroblast population in the development of tissue fibrosis, such as myocardial, renal and liver fibrosis [24]. TGF-b1-induced EMT can promote myofibroblast transformation, which is prominently involved in the fibrotic processes [9].…”