About this Research Topic
Cardiovascular diseases (CVDs) are the leading causes of morbidity worldwide. It is well-accepted that mitochondrial dysregulation and oxidative stress play key roles in a host of cardiac diseases, including atherosclerosis, ischemia/reperfusion injury, cardiac hypertrophy， heart failure and stroke. Oxidative stress is related to the imbalance between the production of reactive oxygen species (ROS) and the availability of antioxidants. Moreover, ROS production is thought to contribute significantly to cardiac pathology. There are accumulating studies demonstrating that mitochondria-targeted molecules as therapeutic targets can be prominent strategies to treat cardiac diseases.
Ferroptosis is an iron-dependent cell death and its genetic, biochemical, morphological characteristics are distinct from apoptosis, necroptosis, pyroptosis and autophagy-dependent cell death. During ferroptosis, a large amount of iron accumulation is accompanied by ROS overproduction, which leads to oxidative modification of lipids in cellular membrane structure, and ultimately cell death. Ferroptosis plays a critical role in the regulation of oxidative stress and inflammatory responses. Therefore, targeting ferroptosis will provide new insights to prevention and treatment of CVDs.
This series aims to highlight the normal mechanisms of oxidative stress, mitochondrial dysfunction and ferroptosis, investigating the pathological and physiological connections between mitochondria and CVDs.
We welcome submissions that focus on, but are not limited to, the following areas:
The role of oxidative stress, especially mitochondrial ROS production in CVDs, and the antioxidant therapies for CVDs.
The roles and mechanisms of mitochondrial dysfunction in CVDs.
The potential roles and mechanisms of ferroptosis in CVDs, as well as the research regarding targeting ferroptosis as a novel therapeutic approach against CVDs.
The interplay between oxidative stress and mitochondrial dysfunction, oxidative stress and ferroptosis or mitochondrial dysfunction and ferroptosis, as well as their connections in CVDs.
We also encourage other progresses in CVDs.
Ferroptosis is an iron-dependent cell death and its genetic, biochemical, morphological characteristics are distinct from apoptosis, necroptosis, pyroptosis and autophagy-dependent cell death. During ferroptosis, a large amount of iron accumulation is accompanied by ROS overproduction, which leads to oxidative modification of lipids in cellular membrane structure, and ultimately cell death. Ferroptosis plays a critical role in the regulation of oxidative stress and inflammatory responses. Therefore, targeting ferroptosis will provide new insights to prevention and treatment of CVDs.
This series aims to highlight the normal mechanisms of oxidative stress, mitochondrial dysfunction and ferroptosis, investigating the pathological and physiological connections between mitochondria and CVDs.
We welcome submissions that focus on, but are not limited to, the following areas:
The role of oxidative stress, especially mitochondrial ROS production in CVDs, and the antioxidant therapies for CVDs.
The roles and mechanisms of mitochondrial dysfunction in CVDs.
The potential roles and mechanisms of ferroptosis in CVDs, as well as the research regarding targeting ferroptosis as a novel therapeutic approach against CVDs.
The interplay between oxidative stress and mitochondrial dysfunction, oxidative stress and ferroptosis or mitochondrial dysfunction and ferroptosis, as well as their connections in CVDs.
We also encourage other progresses in CVDs.
Keywords: Cardiovascular diseases, mitochondrial dysfunction, oxidative stress, reactive oxygen species, ferroptosis
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.
