Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, necessitating a deeper understanding of their underlying mechanisms. Recent research has highlighted the pivotal roles of oxidative stress and mitochondrial dysfunction in the pathogenesis of various cardiac conditions, such as atherosclerosis, ischemia/reperfusion injury, cardiac hypertrophy, heart failure, and stroke. Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, contributing significantly to cardiac pathology. Emerging studies suggest that targeting mitochondria with specific molecules could offer promising therapeutic strategies for cardiac diseases. Additionally, ferroptosis, a distinct form of iron-dependent cell death, has been identified as a critical regulator of oxidative stress and inflammatory responses in CVDs. Despite these advances, the intricate relationships between oxidative stress, mitochondrial dysfunction, and ferroptosis in CVDs remain inadequately explored, highlighting the need for further investigation.
This research topic aims to elucidate the normal and pathological mechanisms of oxidative stress, mitochondrial dysfunction, and ferroptosis in cardiovascular diseases. By exploring these interconnected pathways, the research seeks to uncover novel insights into the prevention and treatment of CVDs. Key objectives include understanding the role of mitochondrial ROS production in CVDs, investigating antioxidant therapies, and examining the potential of targeting ferroptosis as a therapeutic approach. The research will also delve into the interplay between oxidative stress, mitochondrial dysfunction, and ferroptosis, aiming to clarify their collective impact on cardiovascular health.
To gather further insights into the complex interactions between oxidative stress, mitochondrial dysfunction, and ferroptosis in cardiovascular diseases, we welcome articles addressing, but not limited to, the following themes:
- The role of oxidative stress, particularly mitochondrial ROS production, in CVDs, and the development of antioxidant therapies.
- The mechanisms and implications of mitochondrial dysfunction in CVDs.
- The potential roles and mechanisms of ferroptosis in CVDs, including research on targeting ferroptosis as a novel therapeutic strategy.
- The interplay between oxidative stress and mitochondrial dysfunction, oxidative stress and ferroptosis, or mitochondrial dysfunction and ferroptosis, and their connections in CVDs.
- Other advancements and progress in understanding and treating CVDs.
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, necessitating a deeper understanding of their underlying mechanisms. Recent research has highlighted the pivotal roles of oxidative stress and mitochondrial dysfunction in the pathogenesis of various cardiac conditions, such as atherosclerosis, ischemia/reperfusion injury, cardiac hypertrophy, heart failure, and stroke. Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, contributing significantly to cardiac pathology. Emerging studies suggest that targeting mitochondria with specific molecules could offer promising therapeutic strategies for cardiac diseases. Additionally, ferroptosis, a distinct form of iron-dependent cell death, has been identified as a critical regulator of oxidative stress and inflammatory responses in CVDs. Despite these advances, the intricate relationships between oxidative stress, mitochondrial dysfunction, and ferroptosis in CVDs remain inadequately explored, highlighting the need for further investigation.
This research topic aims to elucidate the normal and pathological mechanisms of oxidative stress, mitochondrial dysfunction, and ferroptosis in cardiovascular diseases. By exploring these interconnected pathways, the research seeks to uncover novel insights into the prevention and treatment of CVDs. Key objectives include understanding the role of mitochondrial ROS production in CVDs, investigating antioxidant therapies, and examining the potential of targeting ferroptosis as a therapeutic approach. The research will also delve into the interplay between oxidative stress, mitochondrial dysfunction, and ferroptosis, aiming to clarify their collective impact on cardiovascular health.
To gather further insights into the complex interactions between oxidative stress, mitochondrial dysfunction, and ferroptosis in cardiovascular diseases, we welcome articles addressing, but not limited to, the following themes:
- The role of oxidative stress, particularly mitochondrial ROS production, in CVDs, and the development of antioxidant therapies.
- The mechanisms and implications of mitochondrial dysfunction in CVDs.
- The potential roles and mechanisms of ferroptosis in CVDs, including research on targeting ferroptosis as a novel therapeutic strategy.
- The interplay between oxidative stress and mitochondrial dysfunction, oxidative stress and ferroptosis, or mitochondrial dysfunction and ferroptosis, and their connections in CVDs.
- Other advancements and progress in understanding and treating CVDs.