Dedifferentiation and Redifferentiation in Epithelial Repair

摘要: Acute kidney injury (AKI) occurs in up to 30% of hospitalized patients intensive care units and independently predicts a mortality rate approximately 40%. Most frequently, AKI results from acute tubular necrosis following hypoperfusion the renal proximal (RPT) epithelium. Regeneration is mediated by surviving RPT cells (RPTC) that dedifferentiate, proliferate, migrate, redifferentiate restore damaged epithelial monolayer. Growth factors are required for all four phases regeneration; however, their regulation dedifferentiation/redifferentiation not fully understood. Dedifferentiation characterized loss apical–basal polarity brush border, formation stress fibers, elongated cell morphology, expression mesenchymal proteins. Activation several signal transduction pathways growth factors, including transforming factor-β, epidermal factor, fibroblast factor-2, mediates phenotypic changes dedifferentiation. The mechanism RPTC redifferentiation largely unexplored. current literature suggests bone morphogeneic protein-7, collagen IV, hepatocyte factor mediate through negative drive maintain