FMO5 and chronic obstructive pulmonary disease: It is attributable to various pathophysiological mechanisms involving mitochondrial senescence, NADPH oxidase (NOX) overactivation, endothelial dysfunction, overactivation of the tissue renin-angiotensin-aldosterone system (RAAS), and also to COPD-related hypoxia [1,2,39,54,55,56,57,72].