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Calcium Signaling in Airway Epithelial Cells: Current Understanding and Implications for Inflammatory Airway Disease.
Jairaman, Amit; Prakriya, Murali.
Afiliação
  • Jairaman A; Department of Physiology and Biophysics, School of Medicine, University of California-Irvine (UCI) (A.J.).
  • Prakriya M; Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, IL (M.P.).
Arterioscler Thromb Vasc Biol ; 44(4): 772-783, 2024 Apr.
Article em En | MEDLINE | ID: mdl-38385293
ABSTRACT
Airway epithelial cells play an indispensable role in protecting the lung from inhaled pathogens and allergens by releasing an array of mediators that orchestrate inflammatory and immune responses when confronted with harmful environmental triggers. While this process is undoubtedly important for containing the effects of various harmful insults, dysregulation of the inflammatory response can cause lung diseases including asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis. A key cellular mechanism that underlies the inflammatory responses in the airway is calcium signaling, which stimulates the production and release of chemokines, cytokines, and prostaglandins from the airway epithelium. In this review, we discuss the role of major Ca2+ signaling pathways found in airway epithelial cells and their contributions to airway inflammation, mucociliary clearance, and surfactant production. We highlight the importance of store-operated Ca2+ entry as a major signaling hub in these processes and discuss therapeutic implications of targeting Ca2+ signaling for airway inflammation.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Asma / Sinalização do Cálcio Limite: Humans Idioma: En Revista: Arterioscler Thromb Vasc Biol Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Asma / Sinalização do Cálcio Limite: Humans Idioma: En Revista: Arterioscler Thromb Vasc Biol Ano de publicação: 2024 Tipo de documento: Article