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In addition to impairing cellular macromolecular function, the oxidative stress generated is reported to result in the loss of membrane phospholipids and cholesterol [6,7,8], rearrangement of lipid species [9, 10], and altering membrane protein function [5]

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A 7-point consensus strategy was prepared, which included: (1) enhancing awareness and seriousness of ECOPD, (2) identifying patients at risk for future exacerbations, (3) optimizing pharmacologic treatment of COPD, (4) identifying and treating comorbidities, (5) preventing bacterial and viral infections, (6) pulmonary rehabilitation, and (7) palliative care

Among these thirty-two, twenty-three targets were mapped in cells, including epithelial cells, T helper effector cells, dendritic cells, mast cells, afferent vagal neurons, macrophages, e-NANC neurons, and eosinophils, that are implicated in the molecular pathways involved in airway inflammation