Calzada, María José

Hypoxia in physiopathology: Molecular mechanisms involved in pulmonary diseases

Calzada, María José
Calzada, María José
Hypoxia in physiopathology: Molecular mechanisms involved in pulmonary diseases

Universidad Autónoma of Madrid

School of Medicine. Dept. of Medicine

Phone number
Hypoxia, thrombospondin-1, pulmonary hypertension, COPD
Brief description of the research:

Hypoxia is a well-studied process and a paradigm of responses with different consequences on health and illness. In our group we are interested in studying the biological and molecular processes involved in pulmonary pathologies such as pulmonary arterial hypertension (PAH), chronic obstructive pulmonary disease (COPD) and asthma, in which hypoxia plays an important role. We are interested in the translational aspect to respond to relevant clinical questions in these pathologies. The TSP-1 protein is elevated in the lung of patients with PAH as well as COPD. Our studies have shown the importance of TSP-1 in an organ so exposed to changes and environmental aggressions as the lung, identifying the mechanism by which this protein is induced in hypoxia and some of the multiple mechanisms through which TSP-1 promotes PAH.

Although to date the involvement of TSP-1 in COPD has not been demonstrated, it is likely that high levels of TSP-1 would produce an enrichment in the active forms of TGF-β in the lung, which would stimulate the remodeling of the respiratory tract and pulmonary parenchyma and contribute to the pathogenesis of COPD. However, there is still a clear lack of detailed molecular and cellular studies to unravel the potential of TSP-1 as a prognostic marker or therapeutic target in COPD. Among our interests, we emphasize studying the involvement of TSP-1 in vascular remodeling at both the artery and bronchial tree levels, and the hemodynamic and histological aspects of remodeling and endothelial function, as well as ex vivo vascular electrophysiology in animal models for these pathologies.

5 selected publications:
  1. Labrousse-Arias D, Martínez-Ruiz A, Calzada MJ. Antioxid Redox Signal. 2017 doi: 10.1089/ars.2017.7275.

  2. Rogers NM, Ghimire K, Calzada MJ, Isenberg JS. Cardiovasc Res. 2017 doi: 10.1093/cvr/cvx094.

  3. Labrousse-Arias D, Martínez-Alonso E, Corral-Escariz M, Bienes-Martínez R, Berridy J, Serrano-Oviedo L, Conde E, García-Bermejo ML, Giménez-Bachs JM, Salinas-Sánchez AS, Sánchez-Prieto R, Yao M, Lasa M, Calzada MJ. J Cell Biol. 2017 doi: 10.1083/jcb.201608024.

  4. Rogers NM, Sharifi-Sanjani M, Yao M, Ghimire K, Bienes-Martinez R, Mutchler SM, Knupp HE, Baust J, Novelli EM, Ross M, St Croix C, Kutten JC, Czajka CA, Sembrat JC, Rojas M, Labrousse-Arias D, Bachman TN, Vanderpool RR, Zuckerbraun BS, Champion HC, Mora AL, Straub AC, Bilonick RA, Calzada MJ, Isenberg JS. Cardiovasc Res. 2017 doi: 10.1093/cvr/cvw218.

  5. Labrousse-Arias D, Castillo-González R, Rogers NM, Torres-Capelli M, Barreira B, Aragonés J, Cogolludo Á, Isenberg JS, Calzada MJ. Cardiovasc Res. 2016 doi: 10.1093/cvr/cvv243.