Chronic obstructive pulmonary disease (
COPD) is a major cause of morbidity and mortality worldwide and encompasses
chronic bronchitis and
emphysema. It has been shown that vascular wall remodeling and
pulmonary hypertension (PH) can occur not only in patients with
COPD but also in smokers with normal lung function, suggesting a causal role for vascular alterations in the development of
emphysema. Mechanistically, abnormalities in the vasculature, such as
inflammation, endothelial dysfunction, imbalances in cellular apoptosis/proliferation, and increased oxidative/nitrosative stress promote development of PH,
cor pulmonale, and most probably
pulmonary emphysema.
Hypoxemia in the pulmonary chamber modulates the activation of key
transcription factors and signaling cascades, which propagates
inflammation and infiltration of neutrophils, resulting in
vascular remodeling. Endothelial progenitor cells have angiogenesis capabilities, resulting in transdifferentiation of the smooth muscle cells via aberrant activation of several
cytokines,
growth factors, and
chemokines. The vascular endothelium influences the balance between vaso-constriction and -dilation in the heart. Targeting key players affecting the vasculature might help in the development of new treatment strategies for both PH and
COPD. The present review aims to summarize current knowledge about vascular alterations and production of
reactive oxygen species in
COPD. The present review emphasizes on the importance of the vasculature for the usually parenchyma-focused view of the pathobiology of
COPD.