2023
DOI: 10.1016/j.biopha.2023.114628
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Ivacaftor therapy post myocardial infarction augments systemic inflammation and evokes contrasting effects with respect to tissue inflammation in brain and lung

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Cited by 1 publication
(2 citation statements)
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“…However, wildtype CFTR dysfunction has been associated with accelerated degradation of the CFTR protein. Such wildtype CFTR deprivation in brain, heart, and lung tissues are associated with inflammation and oxidative stress [ 19 ]. CFTR activator ivacaftor is an FAD-approved potentiator of mutated human F508del CFTR .…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…However, wildtype CFTR dysfunction has been associated with accelerated degradation of the CFTR protein. Such wildtype CFTR deprivation in brain, heart, and lung tissues are associated with inflammation and oxidative stress [ 19 ]. CFTR activator ivacaftor is an FAD-approved potentiator of mutated human F508del CFTR .…”
Section: Introductionmentioning
confidence: 99%
“…Unlike human F508del CFTR, ivacaftor does not potentiate mouse F508del cftr [ 20 ]. However, systemic ivacaftor treatment ameliorates hippocampal neuron atrophy in wildtype cftr in mice [ 19 ]. Furthermore, ivacaftor strongly promotes nuclear factor E2-related factor-2 (Nrf2) expression and nuclear translocation in mutated and wildtype human cystic fibrosis bronchial epithelial cells [ 21 ], which further promotes the translation of antioxidative gene elements, including NADPH oxidase 1 ( NOX1 ), quinone oxidoreductase 1 (NQO1), superoxide dismutase 2 ( SOD2 ), and heme oxygenase-1 ( HO1 ) [ 22 - 24 ].…”
Section: Introductionmentioning
confidence: 99%