Mitochondria play crucial roles in biosynthetic, programmed cell death, and signal transduction. The mitochondrial network is dynamic. It undergoes regular fusion and division, together with those processes influenced by a variety of metabolic and cellular signals. Moreover, it regulates many aspects of mitochondrial biology. Mitochondrial dysfunction can drastically alter cell and tissue homeostasis and is increasingly implicated in a series of disorders. Emerging evidence reveals that mitochondria are key hubs in innate immune responses, and mitochondrial constituents (mtDNA, mROS, cardiolipin, ATP, etc.) could promote inflammatory responses.
A growing body of evidence reveals that mitochondrial disorders are related to lung diseases including COPD, asthma, lung injury, ILD, pulmonary fibrosis, and lung cancer. It was demonstrated that in airway cells, mitochondria were related to inflammation, oxidant injury, apoptosis, and innate and adaptive immune responses. However, the regulatory mechanisms of mitochondrial homeostasis in lung diseases are currently unclear. Hence, it will be of great significance to uncover the immuno-regulatory mechanism of mitochondrial dysfunction involved in lung diseases.
This Research Topic aims to shed light on the molecular mechanisms by which mitochondria are involved in inflammation in lung diseases. Herein, this topic particularly focuses on how mitochondria disorders play roles in the progression of lung diseases.
We welcome Original Research articles, Comprehensive Reviews, and Mini-Reviews that cover any aspect of mitochondrial dysfunction of airway cells in lung diseases, including, but not limited to the following topics:
- Mitochondrial metabolic reprogramming in airway inflammation;
- Mitochondrial dysfunction in the immune microenvironment of lung cancer;
- Molecular mechanisms involved in mitochondrial dysfunction in lung diseases;
- Mitochondrial dynamics in lung diseases;
- Regulatory mechanism of mitochondrial in the function of lung leukocytes.
Mitochondria play crucial roles in biosynthetic, programmed cell death, and signal transduction. The mitochondrial network is dynamic. It undergoes regular fusion and division, together with those processes influenced by a variety of metabolic and cellular signals. Moreover, it regulates many aspects of mitochondrial biology. Mitochondrial dysfunction can drastically alter cell and tissue homeostasis and is increasingly implicated in a series of disorders. Emerging evidence reveals that mitochondria are key hubs in innate immune responses, and mitochondrial constituents (mtDNA, mROS, cardiolipin, ATP, etc.) could promote inflammatory responses.
A growing body of evidence reveals that mitochondrial disorders are related to lung diseases including COPD, asthma, lung injury, ILD, pulmonary fibrosis, and lung cancer. It was demonstrated that in airway cells, mitochondria were related to inflammation, oxidant injury, apoptosis, and innate and adaptive immune responses. However, the regulatory mechanisms of mitochondrial homeostasis in lung diseases are currently unclear. Hence, it will be of great significance to uncover the immuno-regulatory mechanism of mitochondrial dysfunction involved in lung diseases.
This Research Topic aims to shed light on the molecular mechanisms by which mitochondria are involved in inflammation in lung diseases. Herein, this topic particularly focuses on how mitochondria disorders play roles in the progression of lung diseases.
We welcome Original Research articles, Comprehensive Reviews, and Mini-Reviews that cover any aspect of mitochondrial dysfunction of airway cells in lung diseases, including, but not limited to the following topics:
- Mitochondrial metabolic reprogramming in airway inflammation;
- Mitochondrial dysfunction in the immune microenvironment of lung cancer;
- Molecular mechanisms involved in mitochondrial dysfunction in lung diseases;
- Mitochondrial dynamics in lung diseases;
- Regulatory mechanism of mitochondrial in the function of lung leukocytes.