Credit: Adobe Stock/ photobyphotoboy
A new study supports a causal link between apolipoprotein A-I (apoA-I) and chronic obstructive pulmonary disease (COPD).1
Preliminary research has identified a potential link between COPD and lipid metabolism. Cigarette smoke extract disrupts lipid metabolism in human bronchial epithelial cells, promoting lipid accumulation via the sphingolipid pathway. From there, phospholipid peroxide buildup in lung epithelial cells triggers ferroptosis, and the disrupted iron homeostasis elevates oxidative stress in COPD, worsening lung tissue damage.2
The involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis suggests the link between COPD and lipid metabolism. It also suggests that abnormal blood lipid levels are…