As research on mitochondria continues to progress, an increasing number of novel exciting functions beyond oxidative phosphorylation and ATP production have been elucidated, including roles in oxidative stress, immune regulation, signal transduction, and cellular fate determination. Consequently, mitochondrial dysfunction has been implicated in a wide range of diseases affecting nearly all human physiological systems. Recent studies have highlighted the potential role of mitochondrial DNA release from damaged mitochondria in triggering low-grade inflammation in various pathological conditions, such as cancer and aging, through the activation of innate immune responses. Therefore, elucidating the mechanisms by which mitochondria link metabolic reprogramming and immune activation in disease is essential in the realm of healthcare. Furthermore, identifying novel targets to restore mitochondrial homeostasis may offer valuable insights for the advancement of preventive and therapeutic approaches for human diseases.
Mitochondrial dysfunction-induced metabolic disorders and low-grade inflammation contribute to the pathogenesis of various diseases. Nevertheless, the precise mechanisms underlying the occurrence of mitochondrial dysfunction, as well as the initiation of metabolic disorders and immune activation by damaged mitochondria, remain poorly understood. Enhancing comprehension of the fundamental genes and mechanisms that govern the interaction between mitochondria, metabolism, and the immune system may offer novel strategies for enhancing mitochondrial function and subsequently restoring metabolic and immune equilibrium. Consequently, the primary objective of this Research Topic is to serve as a forum for researchers concentrating on the intersection of mitochondrial dysfunction, immune response, metabolic alterations, and disease pathogenesis. Our goal is to spotlight recent advancements in understanding how mitochondrial dysfunction contributes to metabolic disorders and immune activation in various diseases. The goal of this theme is to provokes new potential approach for restoring mitochondrial function in order to mitigate metabolic disorders and inflammation, thereby facilitating the advancement of interventions and pharmaceutical treatments for scientific and clinical investigation.
Academic researchers are encouraged to submit manuscripts focusing on the theme and the submission should address various themes related to this topic, including but not limited to:
1. The key genes and mechanisms that induce mitochondrial dysfunction in diseases.
2. The key genes and mechanisms that link mitochondria dysfunction, metabolic disorder and immune activation in diseases.
3. The role of mitochondrial dysfunction-induced metabolic disorder and immune activation on cell injury and cell fate.
4. Targets and methods to alleviate mitochondrial dysfunction, and prevent damaged mitochondria-induced metabolic disorder and immune activation in diseases.
Original research articles, timely reviews or mini reviews, rapid communications and expert perspectives are welcome. It should be noted that manuscripts covering pure bioinformatic analyses are not in scope of the Immunogenetics section of Frontiers in Genetics. Experimental (wet lab) validation of the in silico obtained results is prerequisite for peer-review.
As research on mitochondria continues to progress, an increasing number of novel exciting functions beyond oxidative phosphorylation and ATP production have been elucidated, including roles in oxidative stress, immune regulation, signal transduction, and cellular fate determination. Consequently, mitochondrial dysfunction has been implicated in a wide range of diseases affecting nearly all human physiological systems. Recent studies have highlighted the potential role of mitochondrial DNA release from damaged mitochondria in triggering low-grade inflammation in various pathological conditions, such as cancer and aging, through the activation of innate immune responses. Therefore, elucidating the mechanisms by which mitochondria link metabolic reprogramming and immune activation in disease is essential in the realm of healthcare. Furthermore, identifying novel targets to restore mitochondrial homeostasis may offer valuable insights for the advancement of preventive and therapeutic approaches for human diseases.
Mitochondrial dysfunction-induced metabolic disorders and low-grade inflammation contribute to the pathogenesis of various diseases. Nevertheless, the precise mechanisms underlying the occurrence of mitochondrial dysfunction, as well as the initiation of metabolic disorders and immune activation by damaged mitochondria, remain poorly understood. Enhancing comprehension of the fundamental genes and mechanisms that govern the interaction between mitochondria, metabolism, and the immune system may offer novel strategies for enhancing mitochondrial function and subsequently restoring metabolic and immune equilibrium. Consequently, the primary objective of this Research Topic is to serve as a forum for researchers concentrating on the intersection of mitochondrial dysfunction, immune response, metabolic alterations, and disease pathogenesis. Our goal is to spotlight recent advancements in understanding how mitochondrial dysfunction contributes to metabolic disorders and immune activation in various diseases. The goal of this theme is to provokes new potential approach for restoring mitochondrial function in order to mitigate metabolic disorders and inflammation, thereby facilitating the advancement of interventions and pharmaceutical treatments for scientific and clinical investigation.
Academic researchers are encouraged to submit manuscripts focusing on the theme and the submission should address various themes related to this topic, including but not limited to:
1. The key genes and mechanisms that induce mitochondrial dysfunction in diseases.
2. The key genes and mechanisms that link mitochondria dysfunction, metabolic disorder and immune activation in diseases.
3. The role of mitochondrial dysfunction-induced metabolic disorder and immune activation on cell injury and cell fate.
4. Targets and methods to alleviate mitochondrial dysfunction, and prevent damaged mitochondria-induced metabolic disorder and immune activation in diseases.
Original research articles, timely reviews or mini reviews, rapid communications and expert perspectives are welcome. It should be noted that manuscripts covering pure bioinformatic analyses are not in scope of the Immunogenetics section of Frontiers in Genetics. Experimental (wet lab) validation of the in silico obtained results is prerequisite for peer-review.