To advance the knowledge on molecular pathways of disease and to identify new therapeutic strategies in...


Pulmonary hypertension is a disease characterized by elevated pulmonary arterial pressure due to increased pulmonary vascular resistance. The pathophysiology is complex and involves vasoconstriction, proliferation and thrombosis. The process is initiated with an imbalance between vasoactive factors.  Pulmonary hypertension progresses to heart failure and the prognosis of most forms of the disease is poor. The treatments currently available improve symptoms and quality of life and delay but do not stop the course of the disease. The objective of this line of research is to characterize the effects and mechanisms of action of vasoactive factors that modulate the pulmonary vascular tone, the interactions between them and how they are altered in pathological situations. Our focus is primarily to get a better knowledge of the molecular pathways altered in disease and contribute to vasoconstriction, proliferation and inflammation. We have studied some important mediators such as thromboxane A2, isoprostanes, endothelin-1, angiotensin II and 5-HT, hypoxia and nitric oxide as well as intracellular signalling mechanisms: cytosolic Ca2+, Ca2+ and K+ currents, protein kinases, reactive oxygen species, sphingolipids, cyclic nucleotides and adapter proteins. We analyze the effects of various drugs that interfere with these signaling pathways and that can be potentially useful in the treatment of pulmonary hypertension. 

Our current interest is focused in:

  • The role of vitamin D and the microbiota in pulmonary hypertension.
  • The role of potassium channels TASK1 and Kv7 in pulmonary hypertension and the regulation of their expression by miRNAs.
  • The liver-lung axis. How hepatic exosomes from healthy and cirrhotic animals impact on the lung.