RNA-binding proteins as a molecular link between COPD and pulmonary hypertension

Pulmonary hypertension (PH) is a vascular disease characterized by remodeling of the pulmonary arteries and right heart failure. Chronic obstructive pulmonary disease (COPD) patients often have PH, which can worsen symptoms and raise morbidity and mortality. There are several reasons for increased pulmonary vascular resistance, pulmonary vascular remodeling, and ultimately the development of PH in COPD. These factors include genetics, inflammation caused by chemicals breathed, and changes in the alveoli seen in COPD and its physiology. Genes involved in mRNA conversion, subcellular localization, splicing, and translation are all finely tuned by RBPs in their post-transcriptional regulation. Erythropoietin regulates cytokines, chemokines, proteins, growth factors, and other pro-inflammatory mediators that change the lung microenvironment. Over the past few years, we have learned more about how RBPs act in PH and COPD. Here, we discuss the existing understanding of RBPs' location in the same pathogenic pathways shared by PH and COPD in order to emphasize their potential relevance as disease determinant/biomarker and, consequently, for possible therapeutic targeting.