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Succinate links mitochondria to deadly bacteria in cystic fibrosis
Author(s) -
Speranza Esposito,
Valeria Rachela Villella,
Federica Rossin,
Antonella Tosco,
Valeria Raia,
Alessandro Luciani
Publication year - 2019
Publication title -
annals of translational medicine
Language(s) - English
Resource type - Journals
eISSN - 2305-5847
pISSN - 2305-5839
DOI - 10.21037/atm.2019.12.49
Subject(s) - cystic fibrosis , cystic fibrosis transmembrane conductance regulator , microbiology and biotechnology , function (biology) , mitochondrion , regulator , biology , loss function , bacteria , cell , gene , medicine , genetics , phenotype
Cystic fibrosis (CF) is a life shortening–autosomal recessive disease caused by loss–of–function mutations in the gene encoding the CF transmembrane conductance regulator (CFTR) that transports essential electrolytes in and out of specialized cells (1). The loss of CFTR causes anomalies in the epithelial ion transport, leading to dehydration of cell surfaces and resulting in the accumulation of sticky obstructions that eventually destroy the integrity and physiology of different organ systems (2).

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