ROS-mediated ferroptosis and pyroptosis in cardiomyocytes: An update

Area of Science:

• Cardiology
• Molecular Biology
• Cellular Physiology

Background:

• Cardiomyocytes are crucial for heart function, interacting with other cardiac cells.
• Reactive oxygen species (ROS) are produced by various cellular sources, including mitochondria and NADPH oxidase.
• Physiological ROS levels regulate cardiac development and function, but dysregulation contributes to cardiovascular diseases (CVDs).

Purpose of the Study:

• To systematically review the sources and destinations of ROS in cardiomyocytes.
• To elucidate the molecular mechanisms linking ROS accumulation to cardiomyocyte ferroptosis and pyroptosis.
• To offer new perspectives for CVD research and treatment.

Main Methods:

• Literature review of studies on ROS metabolism in cardiomyocytes.
• Analysis of molecular pathways involved in ROS-induced cell death.
• Synthesis of current understanding of ROS, ferroptosis, and pyroptosis in cardiac pathology.

Main Results:

• ROS are generated by multiple pathways in cardiomyocytes, including mitochondrial respiration and NADPH oxidase.
• Dysregulated ROS metabolism is implicated in CVDs like hypertrophy, ischemia/reperfusion injury, and diabetic cardiomyopathy.
• Oxidative stress-induced ferroptosis and ROS-triggered pyroptosis are significant contributors to cardiomyocyte death in cardiac diseases.

Conclusions:

• Understanding ROS dynamics in cardiomyocytes is critical for comprehending CVD pathogenesis.
• Targeting ROS-mediated ferroptosis and pyroptosis presents a novel therapeutic strategy for heart diseases.
• This review provides a framework for future research into oxidative stress and cardiac cell death.