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Cellular senescence, initially identified as a tumor suppressor mechanism and contributor to aging, is emerging as a potentially significant player in the pathogenesis of endometriosis

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We assume that F1-glutathione complex may be docked into non-catalytic site of GST, affect the structure of catalytic site of GST, and cause the non-competitive inhibition

However, the presence of ketone bodies in the urine suggests that, despite the low CoA, CoA-dependent FA degradation proceeds unimpeded (Fig