"In a series of experiments using mice and human lung tissue, scientists exposed subjects to high CO₂ levels under normal oxygen and pH conditions. Even without signs of inflammation or tissue destruction, the lungs showed significant structural changes, according to the study. These included thickening of airway smooth muscle, increased extracellular matrix (ECM) deposition, and signs of vascular remodeling, all hallmarks of COPD."
""Carbon dioxide has traditionally been viewed as simply a waste product of breathing," Shigemura said. "Because of this, elevated CO₂ in the blood - what we call hypercapnia - has often been tolerated in patients with lung disease, as part of a clinical strategy known as permissive hypercapnia. Our group at Northwestern has been challenging that view." In a series of experiments using mice and human lung tissue, scientists exposed subjects to high CO₂ levels under normal oxygen and pH conditions."
Chronic elevation of blood CO₂ (hypercapnia) can reshape lung architecture, producing airway smooth muscle thickening, increased extracellular matrix deposition, and vascular remodeling characteristic of COPD. These structural changes arise without inflammation or increased cell proliferation and are driven by hypertrophy of existing cells. Lung fibroblasts exposed to high CO₂ adopt myofibroblast-like characteristics linked to fibrosis and tissue stiffening. CO₂ exposure triggers expression of ECM-related genes. Clinical strategies that tolerate permissive hypercapnia may therefore contribute to disease progression, and targeting CO₂-driven pathways could offer new therapeutic opportunities to limit remodeling.
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