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Additionally, macrophages in chronic wounds often fail to switch from a pro-inflammatory phenotype to a pro-healing phenotype, resulting in a feed-forward loop of inflammation that prevents resolution

Although GSH extrusion may provide a simple mechanism to circumvent the normally protective functions of GSH, there is increasing evidence that GSH export is required for activation of specific apoptotic signaling pathways and/or for proper dismantling of cellular components (Coppola and Ghibelli, 2000

its about fostering long-term resilience

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