Both inflammation, autoimmunity, and several other malignancies, share the symptom of tissue damage that perturbs the body's homeostasis and leads to disease. Our understanding of the mechanism which causes damage and triggers disease leads to a common ailment concerning dysfunctional metabolism and particularly dysfunctional mitochondrial activity. Mitochondria are the cell's power source; therefore, their health is fundamental for the wellness of individual cells and the whole organism. One serious consequence of mitochondrial dysfunction is the excessive generation of intracellular reactive oxygen species or oxidative stress. This can damage the mitochondria perse, alongside the whole cellular machinery in a pathologic vicious cycle scheme. Another consequence is the permeation of mitochondrial-derived nucleic acids into the intracellular and extracellular environment. Potentially, this may enhance proinflammatory type I IFN responses that prevail in some autoimmune conditions. Dysfunctional mitochondria are a putative source of modified self-antigens (autoantigens) that could participate in the generation of autoimmune conditions and generate danger-associated molecular patterns fueling inflammation. More importantly, dysfunctional mitochondria in vital immune cells might interfere in the generation of regulatory networks to prevent, attenuate, or control autoimmune conditions and inflammatory processes.
Research that leads to treatments to improve mitochondrial health might help our ability to alleviate a broad range of diseases where mitochondrial dysfunction has been found, not only autoimmunity and inflammation but also cancer, obesity, aging, etc. Hence the goal of this Research Topic is to engage scientists from the field of autoimmunity and inflammation that would like to contribute their work involving mitochondrial physiology in the broad type of studies done in vitro, in silico, or in vivo models.
We would like this Research Topic to focus on how mitochondrial health is impacted, and the various consequence of their malfunction. We are open to any type of article this journal publishes
accepted by Frontiers in Immunology with a focus on:
• Mitochondria function in inflammation and autoimmune diseases.
• Molecular mechanism upstream or downstream of the mitochondrial dysfunction in inflammation and autoimmunity.
• Novel therapies to improve mitochondrial function in autoimmune and inflammatory diseases.
• How to prevent or revert the mitochondrial dysfunction in diseases where inflammation or autoimmunity are involved.
Both inflammation, autoimmunity, and several other malignancies, share the symptom of tissue damage that perturbs the body's homeostasis and leads to disease. Our understanding of the mechanism which causes damage and triggers disease leads to a common ailment concerning dysfunctional metabolism and particularly dysfunctional mitochondrial activity. Mitochondria are the cell's power source; therefore, their health is fundamental for the wellness of individual cells and the whole organism. One serious consequence of mitochondrial dysfunction is the excessive generation of intracellular reactive oxygen species or oxidative stress. This can damage the mitochondria perse, alongside the whole cellular machinery in a pathologic vicious cycle scheme. Another consequence is the permeation of mitochondrial-derived nucleic acids into the intracellular and extracellular environment. Potentially, this may enhance proinflammatory type I IFN responses that prevail in some autoimmune conditions. Dysfunctional mitochondria are a putative source of modified self-antigens (autoantigens) that could participate in the generation of autoimmune conditions and generate danger-associated molecular patterns fueling inflammation. More importantly, dysfunctional mitochondria in vital immune cells might interfere in the generation of regulatory networks to prevent, attenuate, or control autoimmune conditions and inflammatory processes.
Research that leads to treatments to improve mitochondrial health might help our ability to alleviate a broad range of diseases where mitochondrial dysfunction has been found, not only autoimmunity and inflammation but also cancer, obesity, aging, etc. Hence the goal of this Research Topic is to engage scientists from the field of autoimmunity and inflammation that would like to contribute their work involving mitochondrial physiology in the broad type of studies done in vitro, in silico, or in vivo models.
We would like this Research Topic to focus on how mitochondrial health is impacted, and the various consequence of their malfunction. We are open to any type of article this journal publishes
accepted by Frontiers in Immunology with a focus on:
• Mitochondria function in inflammation and autoimmune diseases.
• Molecular mechanism upstream or downstream of the mitochondrial dysfunction in inflammation and autoimmunity.
• Novel therapies to improve mitochondrial function in autoimmune and inflammatory diseases.
• How to prevent or revert the mitochondrial dysfunction in diseases where inflammation or autoimmunity are involved.