Airway epithelial differentiation and pathogenesis of chronic airway diseases (COPD, asthma, fibrosis, neuroendocrine hyperplasia)[9]

Wellington V. Cardoso
University of Brasilia, Faculty of Medicine (Brazil)
Completed 1981 · Last known relationship

University of Brasilia, Faculty of Medicine (Brazil)
Completed 1981 · Last known relationship
Wellington V. Cardoso's roles include Professor of Medicine (in Genetics and Development) at Columbia University Irving Medical Center; Professor of Medicine (in Genetics and Development); Director, Columbia Center for Human Development; co-PI of the division's T32 in lung science. Medical education: University of Brasilia, Faculty of Medicine (Brazil). Education: University of Sao Paulo (Brazil). Fellowship training: Boston University School of Medicine; University of British Columbia (Canada). Areas of interest include Ontogeny and regulation of the airway stem cell pool in the lung; Lung development and repair-regeneration; developmental signaling (Fgf, Notch, retinoids, Hippo-Yap, microRNAs); Formation and diversification of multiciliated cells in the respiratory system.
Each topic is linked to its supporting source in Sources.
Training includes University of Sao Paulo (Brazil), University of Brasilia, Faculty of Medicine (Brazil), Boston University School of Medicine, and PhD, plus 5 more records.
Explore education and trainingCompleted 1989
Completed 1981
Airway epithelial differentiation and pathogenesis of chronic airway diseases (COPD, asthma, fibrosis, neuroendocrine hyperplasia)[9]
Developmental basis of adult lung disease, including prenatal vitamin A deficiency and postnatal airway hyperresponsiveness[9]
Formation and diversification of multiciliated cells in the respiratory system[9]
Generation of functional lungs by conditional blastocyst complementation (with Munemasa Mori)[9]
Lung development and repair-regeneration; developmental signaling (Fgf, Notch, retinoids, Hippo-Yap, microRNAs)[9]
Ontogeny and regulation of the airway stem cell pool in the lung[9]
SARS-CoV-2-host interactions in the human airway epithelium (single-cell transcriptomics, master-regulator analysis)[9]