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Updated: Sep 12, 2026
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
Relationship between ferroptosis and mitophagy in cardiac ischemia reperfusion injury: a mini-review
Cuihua Liu1, Zunjiang Li2, Botao Li1
1Third-Grade Pharmacological Laboratory on Traditional Chinese Medicine, State Administration of Traditional Chinese Medicine, Medical College, China Three Gorges University, Yichang, Hubei Province, China.
Insights
Myocardial ischemia reperfusion injury (MIRI) involves ferroptosis and mitophagy. Understanding their relationship, particularly via mTOR, NLRP3, and HIF, can improve MIRI treatments and drug development.
Area of Science:
- Cardiovascular research
- Cellular mechanisms of injury
Background:
- Cardiovascular diseases (CVD) pose significant global health challenges.
- Reperfusion therapy for conditions like myocardial infarction can paradoxically cause myocardial ischemia reperfusion injury (MIRI).
- MIRI's pathological processes include ferroptosis and mitophagy, both linked to reactive oxygen species (ROS).
Approach:
- This review examines the intricate relationship between ferroptosis and mitophagy, two key cellular processes implicated in MIRI.
- The roles of key regulators, including mTOR, NLRP3, and HIF, in mediating ferroptosis and mitophagy during MIRI are analyzed.
- The potential for simultaneous regulation of both ferroptosis and mitophagy as a superior therapeutic approach for MIRI is discussed.
Key Points:
- Ferroptosis, a form of regulated cell death, exacerbates MIRI, while mitophagy, a cellular self-cleaning process, can alleviate MIRI.
- Both ferroptosis and mitophagy are linked to reactive oxygen species (ROS), but their precise interplay in MIRI remains incompletely understood.
- The study highlights mTOR, NLRP3, and HIF as critical nodes influencing both ferroptosis and mitophagy in the context of MIRI.
Conclusions:
- Understanding the interplay between ferroptosis and mitophagy is crucial for advancing MIRI treatment.
- Targeting both ferroptosis and mitophagy presents a promising therapeutic avenue for MIRI.
- Further research into drugs modulating these pathways could lead to novel MIRI therapies.
Abstract:
Cardiovascular diseases (CVD), with high morbidity and mortality, seriously affect people's life and social development. Clinically, reperfusion therapy is typically used to treat ischemic cardiomyopathy, such as severe coronary heart disease and acute myocardial infarction. However, reperfusion therapy can lead to myocardial ischemia reperfusion injury (MIRI), which can affect the prognosis of patients. Studying the mechanisms of MIRI can help us improve the treatment of MIRI. The pathological process of MIRI involves many mechanisms such as ferroptosis and mitophagy. Ferroptosis can exacerbate MIRI, and regulation of mitophagy can alleviate MIRI. Both ferroptosis and mitophagy are closely related to ROS, but there is no clear understanding of the relationship between ferroptosis and mitophagy. In this review, we analyzed the relationship between ferroptosis and mitophagy according to the role of mTOR, NLPR3 and HIF. In addition, simultaneous regulation of mitophagy and ferroptosis may be superior to single therapy for MIRI. We summarized potential drugs that can regulate mitophagy and/or ferroptosis, hoping to provide reference for the development of drugs and methods for MIRI treatment.
