Chronic obstructive pulmonary disease (COPD) is a heterogeneous lung disease that is associated with long-term cigarette smoking and represents the third-leading cause of death worldwide (Quaderi and Hurst, 2018). The cellular and molecular determinants underpinning the pathogenesis of COPD remain to be fully understood, but the current thought is that long-term inflammation serves as a driver of remodeling and parenchymal destruction in the proximal airways and distal lung tissue leading to the disease states of chronic bronchitis and emphysema (Hogg et al., 2004). Current disease-modifying therapies are limited in their ability to halt the progression of COPD and in relieving symptoms of dyspnea and airflow obstruction.
Recent investigations have uncovered the functional role for vascular endothelial cells (ECs) in organ regeneration and repair in multiple model systems (Rafii et al., 2016; Augustin and Koh, 2017). ECs maintain highly adaptable cellular functions that promote the development of organ-specific vascular niches that are critical to the maintenance of tissue homeostasis. Through the release of growth factors, known as angiocrine factors, vascular ECs coordinate propagation, patterning, and behavior of adjacent parenchymal and mesenchymal cells within a given tissue type (Rafii et al., 2016; Cao et al., 2014; Ding et al., 2011; Cao et al., 2017; Ding et al., 2014). By contrast, maladaptive ECs that emerge from environments of chronic cellular stresses and injury drive the development of fibrosis or tumorigenesis (Cao et al., 2014). Lung-specific endothelium has been shown to encourage alveologenesis following injury through the release of known angiocrine factors, such as metalloprotease-14 (MMP-14) and bone morphogenetic protein 4 (BMP4; Ding et al., 2011; Lee et al., 2014). As such, harnessing the regenerative potential of the endothelium through delivery of healthy ECs has therapeutic potential in diseased lungs.
CT scan 10 weeks ago showed pulmonary fibrosis and emphysema.
Interesting research?
