About this Research Topic
The coupling of mitochondrial respiration, electron transport chain, and oxidative phosphorylation interfere with the pathological changes of cardiovascular disease. Mitochondria are the main sites of various cell functions and energy generation. Mitochondrial function has become a common feature of these pathological disorders in the development of cardiovascular disease. The contribution of mitochondrial function to myocardial remodeling, myocardial ischemia, and vascular injury has also been highlighted in previous studies.
Recently, it is demonstrated that mitochondrial structural disorder precedes mitochondria dysfunction. With the increase of mitochondrial fission, mitochondrial membrane potential (MMP) decreased, mitochondrial reactive oxygen species (mtROS) production increased, and mitochondria-dependent apoptotic pathways are activated. The superoxide from mitochondria induces the oxidation of tetrahydrobiodin to dihydrobiodin, thus preventing the binding of tetrahydrobiodrin to endothelial nitric oxide synthase (eNOS), thereby reducing the production of nitric oxide by decoupling eNOS. In addition, apoptosis is promoted by activated members of the Caspase family when mitochondrial pro-apoptotic proteins such as cytochrome C and Smac enter the cytoplasm. Mitochondria also participate in the mobilization, senescence, growth and proliferation of cardiomyocytes, fibroblasts and endothelial cells.
Therefore, mitochondrial structural disorder is considered to be a progressive condition and the associated pathophysiological processes are described. However, there are still many aspects in cardiovascular disease that are not fully understood or unknown.
This Research Topic welcomes both original research and reviews pertaining to the mitochondrial structural and function disorder in cardiovascular diseases. We welcome submissions of the following subtopics, but not limited to:
• The regulation of mitochondrial structure and function in the progression of cardiovascular disease.
• Mitochondrial function and oxidative phosphorylation disorder of cardiovascular diseases based on clinical big data mining or bio-informatics analysis.
• Regulatory relationship between new cell death modes, includes ferroptosis and copper induces cell death.
• Regulation mechanism of mitochondrial DNA content and the activity of mitochondrial respiratory chain complexes under the pathological stress of cardiovascular disease.
Recently, it is demonstrated that mitochondrial structural disorder precedes mitochondria dysfunction. With the increase of mitochondrial fission, mitochondrial membrane potential (MMP) decreased, mitochondrial reactive oxygen species (mtROS) production increased, and mitochondria-dependent apoptotic pathways are activated. The superoxide from mitochondria induces the oxidation of tetrahydrobiodin to dihydrobiodin, thus preventing the binding of tetrahydrobiodrin to endothelial nitric oxide synthase (eNOS), thereby reducing the production of nitric oxide by decoupling eNOS. In addition, apoptosis is promoted by activated members of the Caspase family when mitochondrial pro-apoptotic proteins such as cytochrome C and Smac enter the cytoplasm. Mitochondria also participate in the mobilization, senescence, growth and proliferation of cardiomyocytes, fibroblasts and endothelial cells.
Therefore, mitochondrial structural disorder is considered to be a progressive condition and the associated pathophysiological processes are described. However, there are still many aspects in cardiovascular disease that are not fully understood or unknown.
This Research Topic welcomes both original research and reviews pertaining to the mitochondrial structural and function disorder in cardiovascular diseases. We welcome submissions of the following subtopics, but not limited to:
• The regulation of mitochondrial structure and function in the progression of cardiovascular disease.
• Mitochondrial function and oxidative phosphorylation disorder of cardiovascular diseases based on clinical big data mining or bio-informatics analysis.
• Regulatory relationship between new cell death modes, includes ferroptosis and copper induces cell death.
• Regulation mechanism of mitochondrial DNA content and the activity of mitochondrial respiratory chain complexes under the pathological stress of cardiovascular disease.
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.
