About this Research Topic
Ischemic cardiovascular disease (CVD) is a leading cause of mortality worldwide. An estimated 18 million people died from CVDs in 2019, representing 32% of all global deaths. Of these deaths, 85% were due to heart attack and stroke. All CVDs eventually progress to heart failure (HF) if not effectively treated. HF affects 1–2% of the world’s population and places a heavy burden on society. Ferroptosis plays a crucial role in CVD pathogenesis. Proper mitochondrial function is necessary in tissues and organs that are of high energy demand, including the heart. CVD is associated with altered mitochondrial biogenesis and clearance. In CVD, impaired mitochondrial function including Ferroptosis results in decreased adenosine triphosphate production and enhanced reactive oxygen species formation.
Current heart disease treatments, such as healthy lifestyle habits, medications, surgery, and other procedures are dependent on the cause and type of heart damage. Although the above methods alleviate the symptoms of the disease and reduce the mortality rate, some methods have specific drawbacks. The mechanisms of the progression of CVD remains unclear. Ferroptosis is a form of regulated cell death that is characterized by iron overload, leading to the accumulation of lethal levels of lipid hydroperoxides. The metabolism of iron, lipids, amino acids, and glutathione tightly controls the initiation and execution of ferroptosis. In recent years, ferroptosis has been found to play critical roles in cardiomyopathy, myocardial infarction, ischemia/reperfusion injury and HF. This Research Topic includes the mechanisms by which ferroptosis is initiated and controlled and covers ferroptosis as a novel therapeutic target for various cardiovascular diseases.
There is an urgent and unmet need to develop a novel, convenient, and efficient approach to the treatment of Ischemia/Reperfusion Injury targeting ferroptosis. Based on the potential mechanism that mitochondrial dysfunction includes ferroptosis in addition to their signaling pathways, transcription, and translation. We wish to introduce a series of topics, such as anti-ferroptosis inhibitors, target-specific cardiovascular diagnosis, and safe treatment.
Current heart disease treatments, such as healthy lifestyle habits, medications, surgery, and other procedures are dependent on the cause and type of heart damage. Although the above methods alleviate the symptoms of the disease and reduce the mortality rate, some methods have specific drawbacks. The mechanisms of the progression of CVD remains unclear. Ferroptosis is a form of regulated cell death that is characterized by iron overload, leading to the accumulation of lethal levels of lipid hydroperoxides. The metabolism of iron, lipids, amino acids, and glutathione tightly controls the initiation and execution of ferroptosis. In recent years, ferroptosis has been found to play critical roles in cardiomyopathy, myocardial infarction, ischemia/reperfusion injury and HF. This Research Topic includes the mechanisms by which ferroptosis is initiated and controlled and covers ferroptosis as a novel therapeutic target for various cardiovascular diseases.
There is an urgent and unmet need to develop a novel, convenient, and efficient approach to the treatment of Ischemia/Reperfusion Injury targeting ferroptosis. Based on the potential mechanism that mitochondrial dysfunction includes ferroptosis in addition to their signaling pathways, transcription, and translation. We wish to introduce a series of topics, such as anti-ferroptosis inhibitors, target-specific cardiovascular diagnosis, and safe treatment.
Keywords: Ischemia/Reperfusion Injury, Ischemia/Reperfusion, Ferroptosis, Mitochondria dysfunction, Cardiovascular disease, Target medicine, Drug Discovery and Pharmacology
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