Possible causes may be that the complications of low activity in patients with COPD weakened the positive stimulation effect of muscle-bone unit [13, 14] and hypoxia in COPD which may decrease ferritinophagy and autophagy flux, inhibited RANKL-induced ferroptosis in osteoclasts, and eventually accelerated bone loss [15]. Here, TNFSF11 is linked to chronic obstructive pulmonary disease.