Reactive oxygen species (ROS) are highly reactive oxygen-containing molecules. While ROS are naturally produced as byproducts of cellular metabolism, excessive ROS production or impaired antioxidant defense mechanisms can have detrimental effects on the cellular, organ, and organism level. Specifically, inborn errors of redox metabolism result from pathogenic variants in genes involved in redox pathways, leading to impaired antioxidant defense systems, abnormal production of ROS, and oxidative stress.
The aim of this Research Topic is to deepen the understanding of inborn errors of redox metabolism both on a pathophysiological and phenotypical level. Despite recent advances, the exact pathomechanisms by which an increase in ROS leads to disturbed cellular processes remain imperfectly understood. Through original studies in patients with IEM of redox metabolism, we aim to generate novel insights into the pathophysiology of redox disease. Furthermore, it is our goal to provide a summary of the current "state of the art". To achieve this broad objective, this Research Topic is open to original research articles, methods articles, systematic and narrative reviews, as well as perspective articles and case reports of exceptional interest. Please be aware that case reports must contain aspects that significantly advance the understanding of redox-related disorders or should have the potential to change the current treatment practice of the respective condition. In addition, case reports must also follow the section guidelines as stated on the Frontiers in Genetics webpage.
In this Research Topic, we provide a forum for both primary research findings and meta-analyses as well as reviews of the current literature in the field of inherited disorders of redox metabolism. Besides submissions on genetic defects of primarily redox-related pathways, studies on secondary changes of redox metabolism in IEM are welcome. This includes mitochondrial disease, peroxisomal disorders, and disorders of trace element metabolism.
Keywords:
Inborn errors of metabolism, Reactive oxygen species, ROS, Redox metabolism, Thiol metabolism, Oxidative stress
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Reactive oxygen species (ROS) are highly reactive oxygen-containing molecules. While ROS are naturally produced as byproducts of cellular metabolism, excessive ROS production or impaired antioxidant defense mechanisms can have detrimental effects on the cellular, organ, and organism level. Specifically, inborn errors of redox metabolism result from pathogenic variants in genes involved in redox pathways, leading to impaired antioxidant defense systems, abnormal production of ROS, and oxidative stress.
The aim of this Research Topic is to deepen the understanding of inborn errors of redox metabolism both on a pathophysiological and phenotypical level. Despite recent advances, the exact pathomechanisms by which an increase in ROS leads to disturbed cellular processes remain imperfectly understood. Through original studies in patients with IEM of redox metabolism, we aim to generate novel insights into the pathophysiology of redox disease. Furthermore, it is our goal to provide a summary of the current "state of the art". To achieve this broad objective, this Research Topic is open to original research articles, methods articles, systematic and narrative reviews, as well as perspective articles and case reports of exceptional interest. Please be aware that case reports must contain aspects that significantly advance the understanding of redox-related disorders or should have the potential to change the current treatment practice of the respective condition. In addition, case reports must also follow the section guidelines as stated on the Frontiers in Genetics webpage.
In this Research Topic, we provide a forum for both primary research findings and meta-analyses as well as reviews of the current literature in the field of inherited disorders of redox metabolism. Besides submissions on genetic defects of primarily redox-related pathways, studies on secondary changes of redox metabolism in IEM are welcome. This includes mitochondrial disease, peroxisomal disorders, and disorders of trace element metabolism.
Keywords:
Inborn errors of metabolism, Reactive oxygen species, ROS, Redox metabolism, Thiol metabolism, Oxidative stress
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.