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Latest advances in drug repurposing for Cystic Fibrosis lung infections
Flaminia Malvezzi-Campeggi<br />
FFC, Ospedale Maggiore, Piazzale Stefani, 37126 Verona, Italy.<br />
Flaminia Malvezzi-Campeggi
Fondazione per la Ricerca sulla Fibrosi Cistica
FFC, Ospedale Maggiore, Piazzale Stefani, 37126 Verona, Italy.
fmalvezzich@gmail.com
Cystic Fibrosis (CF) is a very serious genetic pathology due to the dysfunctional behavior of the Cystic Fibrosis Transmembarne Regulator (CFTR), a membrane protein that is responsible for the transportation of chloride. Defective protein functions are due either to the quantity of the functional CFTR that reaches the membrane or the compromised functionality of the protein. One of the main consequences of the disrupted regulation of chloride ion density is the recurrence and severity of lung infections in CF patients, in which Pseudomonas aeruginosa infections determine loss of lung function. In fact, mucus keeps building up in the lungs because the interchange of chloride and sodium is not working properly thus not creating a suitable environment for the cilia to control the flow.
Madireddy Lab
Genetics Society of America
American Society for Biochemistry and Molecular Biology
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