Hypoxia in Pathophysiology: Molecular mechanisms involved in pulmonary diseases

Pulmonary diseases such as pulmonary arterial hypertension (PAH) or chronic obstructive pulmonary disease (COPD) are pathologies with a high prevalence and morbidity characterized by a decrease in oxygen tension in the blood (hypoxemia) and, in some cases, an exacerbated inflammatory response affecting both the respiratory tract and the pulmonary parenchyma leading to loss of function and pulmonary emphysema. Thrombospondin-1 is a matricellular protein that appear transiently during development and injury responses, but its sustained expression can contribute to chronic disease. This might also be the case in PAH and COPD. Our laboratory is interested in decipher the mechanisms involved in the regulation of this protein under stress such as hypoxia or exposure to tobacco smoke and its functional implications in the development and progression of these pulmonary diseases. In this regard we are interested in studying the mechanisms that regulate important aspects of pulmonary smooth muscle cells and pulmonary fibroblasts, such as contractility, in response of extrinsic stimuli of airway innervation, secreted factors from other airway cell types (epithelium, fibroblasts, immune cells, and vasculature). These represent exciting aspects of basic, translational and even clinical lung research.