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Cellular signalling pathways mediating the pathogenesis of chronic inflammatory respiratory diseases: an update

期刊

INFLAMMOPHARMACOLOGY
卷 28, 期 4, 页码 795-817

出版社

SPRINGER BASEL AG
DOI: 10.1007/s10787-020-00698-3

关键词

Cell signaling; Respiratory diseases; Wnt pathway; Inflammatory

资金

  1. Rebecca L. Cooper Medical Research Foundation
  2. Sydney Partnership for Health, Education, Research and Enterprise (SPHERE)
  3. National Health and Medical Research Council of Australia (NHMRC) [1079187]
  4. Prevent Cancer Foundation (PCF)/International Association for the Study of Lung Cancer (IASLC)
  5. Sydney (International Research Training Program Scholarship (IRTP))

向作者/读者索取更多资源

Respiratory disorders, especially non-communicable, chronic inflammatory diseases, are amongst the leading causes of mortality and morbidity worldwide. Respiratory diseases involve multiple pulmonary components, including airways and lungs that lead to their abnormal physiological functioning. Several signaling pathways have been reported to play an important role in the pathophysiology of respiratory diseases. These pathways, in addition, become the compounding factors contributing to the clinical outcomes in respiratory diseases. A range of signaling components such as Notch, Hedgehog, Wingless/Wnt, bone morphogenetic proteins, epidermal growth factor and fibroblast growth factor is primarily employed by these pathways in the eventual cascade of events. The different aberrations in such cell-signaling processes trigger the onset of respiratory diseases making the conventional therapeutic modalities ineffective. These challenges have prompted us to explore novel and effective approaches for the prevention and/or treatment of respiratory diseases. In this review, we have attempted to deliberate on the current literature describing the role of major cell signaling pathways in the pathogenesis of pulmonary diseases and discuss promising advances in the field of therapeutics that could lead to novel clinical therapies capable of preventing or reversing pulmonary vascular pathology in such patients.

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