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Although the molecular mechanism of BPH have been extensively studied, including a disequilibrium of sex hormone [4], stromal-epithelial interactions [5], cytokins [6], autoimmune [7] and oxidative stress (OS) [8], the exact pathogenesis remains unclear

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Perfusion bioreactors attenuated mitochondrial dysfunction and ER stress resulting in a favorable intracellular redox environment as indicated by improved reduced to oxidized glutathione ratio