The heart is a strong muscular pump that enables tissue and organ perfusion. Therefore, a continuous supply of fresh blood is vital for cardiac function. In coronary artery disease, plaques or thrombi induce rapid occlusion, which restricts blood flow to the heart. The primary effect of coronary artery disease is substantial cardiomyocyte death, which prevents the heart from effectively pumping blood to vital organs.
Mitochondrial quality control (MQC) is a group of adaptive responses that regulate mitochondrial protein turnover, mitochondrial biogenesis, mitochondrial fusion, mitochondrial fission, mitophagy and mitochondria-dependent cell death in cardiovascular system. The main consequences of MQC are the rapid removal of defective mitochondrial debris and the timely replenishment of the mitochondrial network. These biophysical processes protect the mitochondria from damage and therefore attenuate the vulnerability of cardiomyocytes and endothelial cells to stressful conditions including oxidative stress, hypoxia, inflammation, ischemia-reperfusion injury, hyperglycemia, and lipotoxicity. After exposure to stress, cardiomyocytes and endothelial cells employ anti-oxidative factors to neutralize mitochondrial ROS, reduce oxidative stress damage and ensure mitochondrial homeostasis. Concurrently, mitochondrial fission is activated so that damaged mitochondrial fractions can be removed from the mitochondrial network, with the cooperation of mitophagy. In contrast, healthy, long mitochondria can integrate with several small mitochondrial fragments to enhance the resistance of the entire mitochondrial population to stress. When these adaptive responses fail, programmed cell death by apoptosis or necroptosis is activated, and damaged mitochondria become the inducers of cell death, enabling the sequestration of incurable and dysfunctional cardiomyocytes and endothelial cells in cardiovascular system.
Original research and reviews are welcome covering, but not limited to, the following sub-topics:
1. New insights into the mechanisms underlying dysregulated mitochondrial quality control in the pathogenesis of myocardial and microvascular injuries.
2. The roles of oxidative stress, mitochondrial fission, mitochondrial fusion, mitochondrial biogenesis, mitophagy, mitochondria-induced death, and mitochondrial unfolded protein response in myocardial and microvascular damages.
3. Mitochondria-targeted approaches (such as melatonin or mitochondria-derived peptides) to attenuate the vulnerability of cardiomyocytes and endothelial cells to stressful conditions including oxidative stress, hypoxia, inflammation, ischemia-reperfusion injury, hyperglycemia, and lipotoxicity.
4. Clinical relevant information on the effects of therapies for myocardium and micro-vessels with a focus on mitochondria.
5. Review of novel approaches to modulate mitochondrial integrity and thus improve cardiovascular function during stressful conditions.
The heart is a strong muscular pump that enables tissue and organ perfusion. Therefore, a continuous supply of fresh blood is vital for cardiac function. In coronary artery disease, plaques or thrombi induce rapid occlusion, which restricts blood flow to the heart. The primary effect of coronary artery disease is substantial cardiomyocyte death, which prevents the heart from effectively pumping blood to vital organs.
Mitochondrial quality control (MQC) is a group of adaptive responses that regulate mitochondrial protein turnover, mitochondrial biogenesis, mitochondrial fusion, mitochondrial fission, mitophagy and mitochondria-dependent cell death in cardiovascular system. The main consequences of MQC are the rapid removal of defective mitochondrial debris and the timely replenishment of the mitochondrial network. These biophysical processes protect the mitochondria from damage and therefore attenuate the vulnerability of cardiomyocytes and endothelial cells to stressful conditions including oxidative stress, hypoxia, inflammation, ischemia-reperfusion injury, hyperglycemia, and lipotoxicity. After exposure to stress, cardiomyocytes and endothelial cells employ anti-oxidative factors to neutralize mitochondrial ROS, reduce oxidative stress damage and ensure mitochondrial homeostasis. Concurrently, mitochondrial fission is activated so that damaged mitochondrial fractions can be removed from the mitochondrial network, with the cooperation of mitophagy. In contrast, healthy, long mitochondria can integrate with several small mitochondrial fragments to enhance the resistance of the entire mitochondrial population to stress. When these adaptive responses fail, programmed cell death by apoptosis or necroptosis is activated, and damaged mitochondria become the inducers of cell death, enabling the sequestration of incurable and dysfunctional cardiomyocytes and endothelial cells in cardiovascular system.
Original research and reviews are welcome covering, but not limited to, the following sub-topics:
1. New insights into the mechanisms underlying dysregulated mitochondrial quality control in the pathogenesis of myocardial and microvascular injuries.
2. The roles of oxidative stress, mitochondrial fission, mitochondrial fusion, mitochondrial biogenesis, mitophagy, mitochondria-induced death, and mitochondrial unfolded protein response in myocardial and microvascular damages.
3. Mitochondria-targeted approaches (such as melatonin or mitochondria-derived peptides) to attenuate the vulnerability of cardiomyocytes and endothelial cells to stressful conditions including oxidative stress, hypoxia, inflammation, ischemia-reperfusion injury, hyperglycemia, and lipotoxicity.
4. Clinical relevant information on the effects of therapies for myocardium and micro-vessels with a focus on mitochondria.
5. Review of novel approaches to modulate mitochondrial integrity and thus improve cardiovascular function during stressful conditions.
