What is it about?
In this review we discuss the effects of the CFTR activity in modulation of mitochondrial functions and cellular ROS levels
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Why is it important?
The CFTR failure induces Cl- accumulation which in turn stimulates IL1B secretion, creating an autocrine positive feedback loop that enhances its own expression, leading to decreased mitochondrial Complex I activity and increased cellular ROS levels (oxidative stress).
Perspectives
We need to understand the underlying mechanism by which Cl- increases IL1B secretion, increases ROS levels and reduces mitochondrial functions. A better understanding of the CFTR signaling pathway may help to find new drugs to improve the cellular failures induced by the reduced CFTR activity in cystic fibrosis, EPOC, asthma, and related diseases (inflammation, cancer, etc.).
Dr Tomás A. Santa Coloma
Institute for Biomedical Research (BIOMED), CONICET, UCA
Read the Original
This page is a summary of: CFTR activity and mitochondrial function, Redox Biology, January 2013, Elsevier,
DOI: 10.1016/j.redox.2012.11.007.
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