Carotid body oxygen sensing and adaptation to hypoxia
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  • 作者:José López-Barneo ; David Macías…
  • 关键词:Oxygen sensing ; Carotid body ; Acclimatization to hypoxia ; Neural crest ; derived stem cells ; Carotid body pathophysiology
  • 刊名:Pfl¨¹gers Archiv - European Journal of Physiology
  • 出版年:2016
  • 出版时间:January 2016
  • 年:2016
  • 卷:468
  • 期:1
  • 页码:59-70
  • 全文大小:1,480 KB
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  • 作者单位:José López-Barneo (1) (2) (3)
    David Macías (1) (2)
    Aida Platero-Luengo (1) (2)
    Patricia Ortega-Sáenz (1) (2) (3)
    Ricardo Pardal (1) (2)

    1. Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Avenida Manuel Siurot s/n, 41013, Seville, Spain
    2. Departamento de Fisiología Médica y Biofísica, Facultad de Medicina, Universidad de Sevilla, Seville, Spain
    3. Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain
  • 刊物主题:Human Physiology;
  • 出版者:Springer Berlin Heidelberg
  • ISSN:1432-2013
文摘
The carotid body (CB) is the principal arterial chemoreceptor that mediates the hyperventilatory response to hypoxia. Our understanding of CB function and its role in disease mechanisms has progressed considerably in the last decades, particularly in recent years. The sensory elements of the CB are the neuron-like glomus cells, which contain numerous transmitters and form synapses with afferent sensory fibers. The activation of glomus cells under hypoxia mainly depends on the modulation of O2-sensitive K+ channels which leads to cell depolarization and the opening of Ca2+ channels. This model of sensory transduction operates in all mammalian species studied thus far, including man. However, the molecular mechanisms underlying the modulation of ion channel function by changes in the O2 level are as yet unknown. The CB plays a fundamental role in acclimatization to sustained hypoxia. Mice with CB atrophy or patients who have undergone CB resection due to surgical treatments show a marked intolerance to even mild hypoxia. CB growth under hypoxia is supported by the existence of a resident population of neural crest-derived stem cells of glia-like phenotype. These stem cells are not highly affected by exposure to low O2 tension; however, there are abundant synapse-like contacts between the glomus cells and stem cells (chemoproliferative synapses), which may be needed to trigger progenitor cell proliferation and differentiation under hypoxia. CB hypo- or hyper-activation may also contribute to the pathogenesis of several prevalent human diseases. Keywords Oxygen sensing Carotid body Acclimatization to hypoxia Neural crest-derived stem cells Carotid body pathophysiology
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