Postdoctoral Research Associate. Funded by MRC.

David studied Biology in the Universidad de Jaén, Spain. As undergraduate he joined Francisco Luque’s lab and became interested in designing new gene therapy tools for the treatment of AIDS, which also was the focus of his PhD. After the completion of his PhD, he carried out a compelling postdoctoral work first in Prof. José López-Barneo’s lab (2009-2014) at the Instituto de Biomedicina de Sevilla (IBiS), and then in Prof. Randall Johnson’s lab (2014-2018) at the Department of Physiology, Development and Neuroscience (PDN) in the University of Cambridge. In this productive postdoctoral period, he was interested in the crosstalk between oxygen sensing systems and the physiological responses to oxygen shifts. In 2018, he joined Muñoz-Espín’s laboratory at the Hutchison/MRC research Centre (Department of Oncology, University of Cambridge) and his work focuses on the role of senescence-induced plasticity at the origin of lung cancer.

Selected publications

  •  Targeting HIF2α-ARNT hetero-dimerisation as a novel therapeutic strategy for Pulmonary Arterial Hypertension
    D. Macias, S. Moore, A. Crosby, M. Southwood, X. Du, H. Tan, S. Xie, A. Vassallo, A.J. Wood, E.M. Wallace, A. S. Cowburn.
    European Respiratory Journal, 10.1183/13993003.02061-2019, 2020.

  • Galacto-conjugation of Navitoclax as an efficient strategy to increase senolytic specificity and reduce platelet toxicity.
    E. González-Gualda†, M. Pàez-Ribes,†, B. Lozano-Torres,†, D. Macias, J. R Wilson III, C. González-López, H-L. Ou, S. Mirón-Barroso, Z. Zhang, A. Lérida-Viso, J. F Blandez, A. Bernardos, F. Sancenón, M. Rovira, L. Fruk, M. Serrano, G. J Doherty, R. Martínez-Máñez*, D. Muñoz-Espín*. 
    Aging Cell. 00:e13142, 2020.

  • HIF-2a is essential for carotid body development and function.
    David Macías, Andrew S. Cowburn, Hortensia Torres-Torrelo, Patricia Ortega-Sáenz, José López-Barneo, Randall S. Johnson.

    HIF-2a is essential for carotid body development and function.
    eLife 7: e34681-2018.

  • An HIF-1α/VEGF-A Axis in Cytotoxic T Cells Regulates Tumor Progression.
    Asis Palazon; Petros A Tyrakis; David Macías; Pedro Veliça; Helene Rundqvist; Susan Fitzpatrick; Nikola Vojnovic; Anthony T Phan; Niklas Loman; Ingrid Hedenfalk; Thomas Hatschek; John Lövrot; Theodoros Foukakis; AnandaW Goldrath; Jonas Bergh; Randall S Johnson.
    Cancer cell. 32 - 5, pp. 669. 13/11/2017. ISSN 1878-3686

  • Cardiovascular adaptation to hypoxia and the role of peripheral resistance.
    Andrew S Cowburn; David Macias; Charlotte Summers; Edwin R Chilvers; Randall S Johnson.
    eLife. 6, 19/10/2017. ISSN 2050-084X

  • Selective accumulation of biotin in arterial chemoreceptors: requirement for carotid body exocytotic dopamine secretion.
    Patricia Ortega Sáenz*; David Macías*; Konstantin L Levitsky; José A Rodríguez Gómez; Patricia González Rodríguez; Victoria Bonilla Henao; Ignacio Arias Mayenco; José López Barneo.
    The Journal of Physiology. 594 - 24, pp. 7229 - 7248. 15/12/2016. ISSN 1469-7793

  •  S-2-hydroxyglutarate regulates CD8+ T-lymphocyte fate.
    Petros A Tyrakis; Asis Palazon; David Macias; Kian L Lee; Anthony T Phan; Pedro Veliça; Jia You; Grace S Chia; Jingwei Sim; Andrew Doedens; Alice Abelanet; Colin E Evans; John R Griffiths; Lorenz Poellinger; Ananda W Goldrath; Randall S Johnson.
    Nature. 540 - 7632, pp. 236- 241. 08/12/2016. ISSN 1476-4687

  • HIF2α-arginase axis is essential for the development of pulmonary hypertension.
    Andrew S Cowburn; Alexi Crosby; David Macias; Cristina Branco; Renato D D R Colaço; Mark Southwood; Mark Toshner; Laura E Crotty Alexander; Nicholas W Morrell; Edwin R Chilvers; Randall S Johnson.
    PNAS. 113 - 31, pp. 8801 - 8806. 02/08/2016. ISSN 1091-6490

  • Deletion of the von Hippel-Lindau gene causes sympathoadrenal cell death and impairs chemoreceptor-mediated adaptation to hypoxia.
    David Macías; Mary Carmen Fernández Agüera; Victoria Bonilla Henao; José López Barneo.
    EMBO molecular medicine. 6 - 12, pp. 1577 - 1592. 12/2014. ISSN 1757-4684

  • A lentiviral vector that activates latent human immunodeficiency virus-1 proviruses by the overexpression of tat and that kills the infected cells..
    David Macías; Ricardo Oya; Luisa Saniger; Francisco Martín; Francisco Luque.
    Human gene therapy. 20 - 11, pp. 1259 - 1268. 11/2009. ISSN 1557-7422