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Editorial
. 2019 Dec;7(Suppl 8):S263.
doi: 10.21037/atm.2019.12.49.

Succinate links mitochondria to deadly bacteria in cystic fibrosis

Speranza Esposito  1 , Valeria Rachela Villella  1 , Federica Rossin  2 , Antonella Tosco  3 , Valeria Raia  1   3 , Alessandro Luciani  4
Affiliations
Editorial

Succinate links mitochondria to deadly bacteria in cystic fibrosis

Speranza Esposito et al. Ann Transl Med. 2019 Dec.
No abstract available

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
CFTR-PTEN dysfunctions drive mitochondrial metabolic defects that sustain Pseudomonas aeruginosa lung infection in CF. In wild type lung cells (left), the functional CFTR-PTEN axis preserves the mitochondrial energy metabolism, hence the homeostasis of the host immune system. In cystic fibrosis affected lung cells (right), the loss of CFTR-PTEN alliance triggers anomalies in the mitochondrial functionality and homeostasis, leading to ROS overproduction and activation of a compensatory antioxidant IRG1 response. This suppresses the mitochondrial SDH activity, resulting in the accumulation of succinate metabolites that feed the P. aeruginosa adaptation and microbial growth, hence promoting persistent infections and inflammation in the lungs of patients with CF.
See this image and copyright information in PMC

Comment on

References

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