ReviewFrontiers in pharmacology2020
Mitochondrial Stress Responses and "Mito-Inflammation" in Cystic Fibrosis.
Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- The importance of mitochondria and mitochondrial calcium signaling in health and disease: an updated outlook on inflammation.Journal of translational medicine · 2026Review
- Redox Imbalance in Cystic Fibrosis: The Multifaceted Role of Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Identifying novel therapeutic targets in cystic fibrosis through advanced single-cell transcriptomics analysis.Computers in biology and medicine · 2025Article
- A New Frontier in Cystic Fibrosis Pathophysiology: How and When Clock Genes Can Affect the Inflammatory/Immune Response in a Genetic Disease Model.Current issues in molecular biology · 2024Review
- The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases.International journal of molecular sciences · 2023Review
- Loss of CFTR function in macrophages alters the cell transcriptional program and delays lung resolution of inflammation.Frontiers in immunology · 2023Article
- The "mitochondrial stress responses": the "Dr. Jekyll and Mr. Hyde" of neuronal disorders.Neural regeneration research · 2022Review
- The Multifaceted Roles of Autophagy in Infectious, Obstructive, and Malignant Airway Diseases.Biomedicines · 2022Review
- Article
- Review
- CD34+ derived macrophage and dendritic cells display differential responses to paraquat.Toxicology in vitro : an international journal published in association with BIBRA · 2021Article
- Promise of the NLRP3 Inflammasome Inhibitors in In Vivo Disease Models.Molecules (Basel, Switzerland) · 2021Review
- Review
- Update on Calcium Signaling in Cystic Fibrosis Lung Disease.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis (CF) is a genetic disease associated to mutations in the cystic fibrosis transmembrane conductance regulator gene, which results in the alteration of biological fluid and electrolyte homeostasis. The characteristic pathological manifestation is represented by exaggerated proinflammatory response in lung of CF patients, driven by recurrent infections and worsen by hypersecretion of proinflammatory mediators and progressive tissue destruction. Treating inflammation remains a priority in CF. However, current anti-inflammatory treatments, including non-steroidal agents, are poorly effective and present dramatic side effects in CF patients. Different studies suggest an intimate relationship between mitochondria and CF lung disease, supporting the hypothesis that a decline in mitochondrial function endorses the development of the hyperinflammatory phenotype observed in CF lung. This allowed the implementation of a new concept: the "mito-inflammation," a compartmentalization of inflammatory process, related to the role of mitochondria in engage and sustain the inflammatory responses, resulting a druggable target to counteract the amplification of inflammatory signals in CF. Here, we will offer an overview of the contribution of mitochondria in the pathogenesis of CF lung disease, delving into mitochondrial quality control responses, which concur significantly to exacerbation of CF lung inflammatory responses. Finally, we will discuss the new therapeutic avenues that aim to target the mito-inflammation, an alternative therapeutic advantage for mitochondrial quality control that improves CF patient's inflammatory state.
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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.