The heart, as the largest energy consumer within the human body, relies primarily on mitochondria for its energy supply. Mitochondrial functionality is significant in heart disease progression, making it crucial to study and develop targeted medications relating to this. Reactive oxygen species (ROS), predominantly originating from mitochondria, can damage biological macromolecules like proteins, subsequently damaging cells and tissue. Mitochondria-targeted drugs can effectively dispel surplus ROS, safeguard mitochondria, and reduce cell damage due to their targeted release into mitochondria. Mitochondria’s role in iron metabolism is essential, where dysfunction could result in iron overload or ferroptosis, encouraging the advancement of heart diseases. Presently, to tackle these diseases, emphasis should be on research into mitochondrial mechanisms and drug development across three aspects: mitochondrial biosynthesis, oxidative stress, and mitochondrial iron utilization.
This Research Topic aims to address the significant issue of heart-related diseases, focusing on their strong links with mitochondrial dysfunction and iron metabolism disorders. It is critical to explore the latest findings in mitochondrial biosynthesis and gauge its role in heart disease pathogenesis, including the effectiveness of associated target drugs. We also aim to consolidate current research on the augmentation of oxidative stress through mitochondrial dysfunction, promoting heart disease progression. Additionally, it is essential to identify mitochondria-targeting drugs that could potentially deter such progression by inhibiting oxidative stress. Lastly, we intend to delve into the complex effects and mechanisms of iron overload or ferroptosis on heart-related diseases, triggered by mitochondrial abnormalities, and to assess the potential prevention of such diseases through medications targeting iron metabolism.
The scope of this Research Topic lies within the area of cardiovascular pharmacology, with an emphasis on the role of mitochondria in heart-related diseases. Potential contributors are invited to address specific themes such as:
• Recent advancements in understanding mitochondrial biosynthesis and its influence on heart-related disease progression.
• Research into the intervention of heart disease progression using mitochondrial synthesis-targeting drugs.
• Mechanistic overviews examining how mitochondrial oxidative stress promotes heart-related diseases.
• Investigations exploring the potential of drug intervention in mitochondrial oxidative stress.
• Studies delving into the mechanism of mitochondrial iron metabolism and its regulation’s role in heart disease progression.
• The influence and mechanics of drugs, inhibitors of mitochondrial iron metabolism, and ferroptosis on heart diseases.
• Updates on research methodologies employed in mitochondrial synthesis, oxidative stress, and iron metabolism.
• Reviews assessing the progress of targeted mitochondrial drugs.
Cardiovascular and Smooth Muscle Pharmacology encourages submission formats including Original Research, Review, Mini Review, Opinion, Perspective, Brief Research Report, and Case Report.
The heart, as the largest energy consumer within the human body, relies primarily on mitochondria for its energy supply. Mitochondrial functionality is significant in heart disease progression, making it crucial to study and develop targeted medications relating to this. Reactive oxygen species (ROS), predominantly originating from mitochondria, can damage biological macromolecules like proteins, subsequently damaging cells and tissue. Mitochondria-targeted drugs can effectively dispel surplus ROS, safeguard mitochondria, and reduce cell damage due to their targeted release into mitochondria. Mitochondria’s role in iron metabolism is essential, where dysfunction could result in iron overload or ferroptosis, encouraging the advancement of heart diseases. Presently, to tackle these diseases, emphasis should be on research into mitochondrial mechanisms and drug development across three aspects: mitochondrial biosynthesis, oxidative stress, and mitochondrial iron utilization.
This Research Topic aims to address the significant issue of heart-related diseases, focusing on their strong links with mitochondrial dysfunction and iron metabolism disorders. It is critical to explore the latest findings in mitochondrial biosynthesis and gauge its role in heart disease pathogenesis, including the effectiveness of associated target drugs. We also aim to consolidate current research on the augmentation of oxidative stress through mitochondrial dysfunction, promoting heart disease progression. Additionally, it is essential to identify mitochondria-targeting drugs that could potentially deter such progression by inhibiting oxidative stress. Lastly, we intend to delve into the complex effects and mechanisms of iron overload or ferroptosis on heart-related diseases, triggered by mitochondrial abnormalities, and to assess the potential prevention of such diseases through medications targeting iron metabolism.
The scope of this Research Topic lies within the area of cardiovascular pharmacology, with an emphasis on the role of mitochondria in heart-related diseases. Potential contributors are invited to address specific themes such as:
• Recent advancements in understanding mitochondrial biosynthesis and its influence on heart-related disease progression.
• Research into the intervention of heart disease progression using mitochondrial synthesis-targeting drugs.
• Mechanistic overviews examining how mitochondrial oxidative stress promotes heart-related diseases.
• Investigations exploring the potential of drug intervention in mitochondrial oxidative stress.
• Studies delving into the mechanism of mitochondrial iron metabolism and its regulation’s role in heart disease progression.
• The influence and mechanics of drugs, inhibitors of mitochondrial iron metabolism, and ferroptosis on heart diseases.
• Updates on research methodologies employed in mitochondrial synthesis, oxidative stress, and iron metabolism.
• Reviews assessing the progress of targeted mitochondrial drugs.
Cardiovascular and Smooth Muscle Pharmacology encourages submission formats including Original Research, Review, Mini Review, Opinion, Perspective, Brief Research Report, and Case Report.
