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Full article: Targeting Non-Eosinophilic Immunological Pathways in COPD and AECOPD: Current Insights and Therapeutic Strategies
Deficiencies in mitochondrial turnover result in heightened lipid ROS production and disrupt iron–sulfur cluster homeostasis, which may diminish the threshold for ferroptotic cellular demise
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doi: 10.1111/j.1600-079x.1997.tb00353.x 76 LivreaMATesoriereLD’ArpaDMorrealeM
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