ReviewRedox biology2013
CFTR activity and mitochondrial function.
Review in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Circulating biomarkers of antioxidant status and oxidative stress in people with cystic fibrosis: A systematic review and meta-analysis.Redox biology · 2020Pooled it
- MITF Regulates CFTR Expression to Participate in Myocardial Ischemia-Reperfusion Injury.The journal of gene medicine · 2026Article
- Review
- The Role of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Enamel Formation.Calcified tissue international · 2026Article
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Intestinal adaptations increase basolateral intestinal glucose uptake and glycolysis in a mouse model of cystic fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Article
- Potential therapeutic role of sex steroids in treating sarcopenia: a network pharmacology and molecular dynamics study.BMC pharmacology & toxicology · 2025Article
- Review
- Loss of CFTR Reverses Senescence Hallmarks in SARS-CoV-2 Infected Bronchial Epithelial Cells.International journal of molecular sciences · 2024Article
- Effects of Exercise Training on Peripheral Muscle Strength in Children and Adolescents with Cystic Fibrosis: A Meta-Analysis.Healthcare (Basel, Switzerland) · 2022Review
- Elexacaftor-Tezacaftor-Ivacaftor improves exercise capacity in adolescents with cystic fibrosis.Pediatric pulmonology · 2022Article
- Carbon nanoparticles adversely affect CFTR expression and toxicologically relevant pathways.Scientific reports · 2022Article
- Article
- Somatic Mutations of Hematopoietic Cells Are an Additional Mechanism of Body Aging, Conducive to Comorbidity and Increasing Chronification of Inflammation.Biomedicines · 2022Review
- Lack of CFTR alters the ferret pancreatic ductal epithelial secretome and cellular proteome: Implications for exocrine/endocrine signaling.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2022Article
- Review
- Cystic fibrosis improves COVID-19 survival and provides clues for treatment of SARS-CoV-2.Purinergic signalling · 2021Article
- NLR family pyrin domain containing 3 (NLRP3) and caspase 1 (CASP1) modulation by intracellular ClImmunology · 2021Article
- miR-125b/NRF2/HO-1 axis is involved in protection against oxidative stress of cystic fibrosis: A pilot study.Experimental and therapeutic medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic Fibrosis (CF) is a frequent and lethal autosomal recessive disease, caused by mutations in the gene encoding the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). Before the discovery of the CFTR gene, several hypotheses attempted to explain the etiology of this disease, including the possible role of a chloride channel, diverse alterations in mitochondrial functions, the overexpression of the lysosomal enzyme α-glucosidase and a deficiency in the cytosolic enzyme glucose 6-phosphate dehydrogenase. Because of the diverse mitochondrial changes found, some authors proposed that the affected gene should codify for a mitochondrial protein. Later, the CFTR cloning and the demonstration of its chloride channel activity turned the mitochondrial, lysosomal and cytosolic hypotheses obsolete. However, in recent years, using new approaches, several investigators reported similar or new alterations of mitochondrial functions in Cystic Fibrosis, thus rediscovering a possible role of mitochondria in this disease. Here, we review these CFTR-driven mitochondrial defects, including differential gene expression, alterations in oxidative phosphorylation, calcium homeostasis, oxidative stress, apoptosis and innate immune response, which might explain some characteristics of the complex CF phenotype and reveals potential new targets for therapy.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.