Pulmonary hypertension is a common co-morbidity of COPD. Previous studies have already established that (in the experimental model) pulmonary vascular changes precede the development of emphysema (destruction of lung tissue, loss of gas exchange capacity). The enzyme iNOS (inducible NO synthase) was identified as a major factor involved.
In a recent study published in the European Respiratory Journal, iNOS in immune cells in particular was shown to play a role in the vascular remodeling underlying PH: In the experimental model (cigarette smoke exposure), cell-specific silencing of the enzyme in these cells was able to exert a protective effect against vascular remodeling (and thus PH), but not against emphysema formation. At the same time, the number of M2-polarized immune cells, as measured by the expression of a specific marker (CD206), was reduced. Interestingly, just such cells (CD206-positive, iNOS-positive) could be found near remodeled pulmonary vessels in tissue preparations from COPD patients.
The results show that different cell types are involved in the development of PH and COPD/emphysema, but they use the same molecular signaling pathway (iNOS).
Further information:
Original publication: Gredic et al., 2021 / European Respiratory Journal
