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Helicobacter pylori activates matrix metalloproteinase 10 in gastric epithelial cells via EGFR and ERK-mediated pathways

when ROS accumulate, they can be released from Nrf2 bound to KEAP1 by an oxidative reaction to increase antioxidant capacity [124, 125]

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These metabolic disturbances not only contribute to the onset of the disease but also accelerate its progression, leading to significant impairment of cardiomyocyte function