New Organ-on-Chip Model Reveals How Airway Injury Triggers Vascular Dysfunction in COPD
Researchers developed REVAS, an organ-on-chip platform that models interactions between respiratory and vascular cells to study how airway injury contributes to cardiovascular complications in COPD. The model shows that oxidative stress in airway cells triggers inflammatory responses and vascular remodeling across multiple cell types, mimicking key features of the disease. This work could help explain the mechanistic links between lung and heart problems in COPD patients and enable testing of new treatments.
Scientists created REVAS, a modular organ-on-chip system containing respiratory chips with airway epithelium and microvascular endothelium, plus a vascular chip with pulmonary artery cells and supporting cells like smooth muscle cells and pericytes. At baseline, the multicellular environment enhanced barrier function and cell differentiation, with mural cells and respiratory cells promoting healthy endothelial function. When exposed to hydrogen peroxide-induced oxidative stress mimicking COPD conditions, the system showed widespread inflammatory gene expression and release of disease-relevant cytokines including IL-6, TNF-β, IL-8, and others. Comparative analysis confirmed that REVAS recapitulates key endothelial dysfunction features observed in actual COPD patients, establishing it as a human-relevant platform for understanding how airway injury drives downstream vascular complications and for evaluating potential therapies.
What's missing
The study's own limitations are not detailed in the abstract provided, such as the scope of cell types tested, duration of oxidative stress exposure, quantitative comparisons to in vivo COPD severity, or timeline for therapeutic validation studies.
What different sources said
- bioRxivCenter
Organ on chip model of respiratory vascular interactions under COPD relevant oxidative stress
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