scispace - formally typeset
S

Speranza Esposito

Researcher at European Institute

Publications -  30
Citations -  1644

Speranza Esposito is an academic researcher from European Institute. The author has contributed to research in topics: Cystic fibrosis transmembrane conductance regulator & Cystic fibrosis. The author has an hindex of 16, co-authored 22 publications receiving 1513 citations. Previous affiliations of Speranza Esposito include University of Foggia & University of Naples Federico II.

Papers
More filters
Journal ArticleDOI

Defective CFTR induces aggresome formation and lung inflammation in cystic fibrosis through ROS-mediated autophagy inhibition

Alessandro Luciani, +18 more
- 01 Sep 2010 - 
TL;DR: It is shown how the defective CFTR results in defective autophagy and decreases the clearance of aggresomes, leading to the accumulation of protein aggregates and to lung inflammation.
Journal ArticleDOI

Targeting the Intracellular Environment in Cystic Fibrosis: Restoring Autophagy as a Novel Strategy to Circumvent the CFTR Defect.

Valeria Rachela Villella, +6 more
- 21 Jan 2013 - 
TL;DR: Recent pre-clinical evidence indicating that targeting the intracellular environment surrounding the misfolded mutant CFTR instead of protein itself could constitute an attractive therapeutic option to sensitize patients carrying the F508del-CFTR mutation to the beneficial action of CFTR potentiators on lung inflammation is reviewed.
Journal ArticleDOI

Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

Daniela De Stefano, +21 more
- 27 Oct 2014 - 
TL;DR: It is reported that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the F508del-CFTR mutation, and optimal schedules of cysteamines plus EGCG might be used for the treatment of CF caused by the F504del- CFTR mutation.
Journal ArticleDOI

Targeting autophagy as a novel strategy for facilitating the therapeutic action of potentiators on ΔF508 cystic fibrosis transmembrane conductance regulator.

Alessandro Luciani, +15 more
- 09 Aug 2012 - 
TL;DR: It is demonstrated that human and mouse CF airways are autophagy deficient due to functional sequestration of BECN1 and that the tissue transglutaminase-2 inhibitor, cystamine, or antioxidants restore BECn1-dependent autophamy and reduce SQSTM1/p62 levels, thus favoring ΔF508-CFTR trafficking to the epithelial surface.
Journal ArticleDOI

A novel treatment of cystic fibrosis acting on-target: cysteamine plus epigallocatechin gallate for the autophagy-dependent rescue of class II-mutated CFTR.

Antonella Tosco, +21 more
- 01 Apr 2016 - 
TL;DR: The proof-of-concept that this combination treatment restored CFTR function and reduced lung inflammation is provided and the results suggest that the combination treatment of cysteamine plus EGCG acts ‘on-target’ because it can only rescueCFTR function when autophagy is functional and improves CFTRfunction when a rescuable protein is expressed.