Abstract
Phosphatidyl inositol 3 kinase gamma (PI3Kγ) is expressed in all the cell types that are involved in airway inflammation and disease, including not only leukocytes, but also structural cells, where it is expressed at very low levels under physiological conditions, while is significantly upregulated after stress. In the airways, PI3Kγ behaves as a trigger or a controller, depending on the pathological context. In this review, the contribution of PI3Kγ in a plethora of respiratory diseases, spanning from acute lung injury, pulmonary fibrosis, asthma, cystic fibrosis and response to both bacterial and viral pathogens, will be commented.
Highlights
Phosphatidyl inositol 3 kinases (PI3Ks) are a family of lipid kinases that play key roles in a plethora of processes, including cell growth, proliferation and differentiation, tissue morphogenesis, metabolism, and immune function
Phosphatidyl inositol 3 kinase gamma (PI3Kγ) is expressed in all the cell types that are involved in airway inflammation and disease, including leukocytes, and structural cells, where it is expressed at very low levels under physiological conditions, while is significantly upregulated after stress
In the past two decades, metabolic dysregulation, impaired mitochondrial autophagy, and mitochondrial dysfunction have been observed in cells of Idiopathic pulmonary fibrosis (IPF) lungs [54]. These results suggest the intriguing hypothesis that the activation level of PI3Kγ might act as a master controller in the different processes that converge on IPF pathogenesis and influence the fate of the lung environment
Summary
Phosphatidyl inositol 3 kinases (PI3Ks) are a family of lipid kinases that play key roles in a plethora of processes, including cell growth, proliferation and differentiation, tissue morphogenesis, metabolism, and immune function. The contribution of PI3Kγ in a plethora of respiratory diseases, spanning from acute lung injury, pulmonary fibrosis, asthma, cystic fibrosis and response to both bacterial and viral pathogens, will be commented. PI3Kγ KO mice display reduced accumulation of neutrophils in an LPS-induced acute lung injury model, and perturbation in E-selectin-mediated adhesion, in response to TNF-α.
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