THE IMPACT OF EPITHELIAL TO MESENCHYMAL TRANSITION IN KIDNEY FIBROSIS

Document Type : Original Article

Authors

1 Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia 61519, Egypt

2 Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia 61519, Egypt /Department of Regenerative Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan

Abstract

Abstract: Fibrosis is a pathological condition attributed to an inappropriate deposition of extracellular matrix that promotes scarring and  dysfunction of the implicated organ or tissue. Moreover, fibrosis encompasses an enormous range of organs and tissues, each with a distinct molecular basis. Yet, two factors are discussed: the critical function of transforming growth factor-beta (TGF-β) and the participation of the inflammatory cascade, which is required to initiate fibrotic destruction. Epithelial to mesenchymal transition (EMT), the most prevalent cellular program underlying  fibrosis, is  regulated by TGF-β, as well as other cytokines. EMT has been widely investigated, although it has not yet been adequately examined as a potential treatment option for fibrosis. A better knowledge of the linkages between fibrosis and EMT may provide an option for the establishment of a highly useful anti-fibrotic treatment. Thus, we provide a general overview of EMT; summarize the significance of TGF-β/Smad signaling cascade in EMT induction, the correlation between both EMT and renal fibrosis and the promising treatment strategies targeting fibrosis induced by EMT.

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