Management of ROS and Regulatory Cell Death in Myocardial Ischemia-Reperfusion Injury

Area of Science:

• Cardiovascular Biology
• Oxidative Stress Research
• Cell Death Mechanisms

Background:

• Myocardial ischemia-reperfusion injury (MIRI) causes significant cardiomyocyte death and cardiac remodeling.
• Reactive oxygen species (ROS) and oxidative stress are key mediators in MIRI pathogenesis.
• ROS exhibit a dual role, maintaining physiological functions at low levels but accelerating damage when excessive.

Purpose of the Study:

• To review the intricate molecular mechanisms linking ROS and regulated cell death (RCD) in cardiomyocytes during MIRI.
• To highlight the potential of targeting ROS to mitigate MIRI-induced cardiomyocyte death.
• To provide insights for developing novel MIRI prevention and treatment strategies.

Main Methods:

• Literature review focusing on molecular pathways of ROS generation and action in MIRI.
• Analysis of studies investigating the interplay between ROS and various RCD types (apoptosis, pyroptosis, autophagy, ferroptosis).
• Examination of therapeutic strategies aimed at ROS reduction for MIRI management.

Main Results:

• Excessive ROS during MIRI triggers diverse molecular pathways leading to cardiomyocyte death.
• ROS actively regulate multiple forms of RCD, including apoptosis, pyroptosis, autophagy, and ferroptosis.
• Antioxidant interventions targeting ROS reduction show promise in alleviating MIRI.

Conclusions:

• Modulating ROS levels is a critical therapeutic target for managing MIRI.
• Understanding the complex ROS-RCD crosstalk offers new avenues for MIRI treatment.
• Further research is needed to translate ROS-targeting strategies from bench to bedside for MIRI patients.