Action of iron chelator on intramyocardial hemorrhage and cardiac remodeling following acute myocardial infarction

Behrouzi, Bita; Weyers, Jill J.; Qi, Xiuling; Barry, Jennifer; Rabadia, Vrajlal; Manca, D.; Connelly, John T.; Spino, Michael; Wood, John C.; Strauss, Bradley H.; Wright, Graham A.; Ghugre, Nilesh R.

doi:10.1007/s00395-020-0782-6

Cited by 40 publications

(16 citation statements)

References 84 publications

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“…Myocardial infarction is characterized by cardiomyocyte death, but the mechanisms are not fully understood, despite basic and clinical research efforts ( Bacmeister et al, 2019 ; Hofbauer et al, 2019 ; Behrouzi et al, 2020 ; Golforoush et al, 2020 ). In the present study, we found that mitochondrial oxidative stress-induced JNK activation may be the upstream trigger of cardiomyocyte death under hypoxic conditions.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction

Cheng

Zheng

et al. 2021

Front. Physiol.

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Myocardial infarction is characterized by cardiomyocyte death, and can be exacerbated by mitochondrial damage and endoplasmic reticulum injury. In the present study, we investigated whether communication between mitochondria and the endoplasmic reticulum contributes to cardiomyocyte death after myocardial infarction. Our data demonstrated that hypoxia treatment (mimicking myocardial infarction) promoted cardiomyocyte death by inducing the c-Jun N-terminal kinase (JNK) pathway. The activation of JNK under hypoxic conditions was dependent on overproduction of mitochondrial reactive oxygen species (mtROS) in cardiomyocytes, and mitochondrial division was identified as the upstream inducer of mtROS overproduction. Silencing mitochondrial division activators, such as B cell receptor associated protein 31 (BAP31) and mitochondrial fission 1 (Fis1), repressed mitochondrial division, thereby inhibiting mtROS overproduction and preventing JNK-induced cardiomyocyte death under hypoxic conditions. These data revealed that a novel death-inducing mechanism involving the BAP31/Fis1/mtROS/JNK axis promotes hypoxia-induced cardiomyocyte damage. Considering that BAP31 is localized within the endoplasmic reticulum and Fis1 is localized in mitochondria, abnormal mitochondria-endoplasmic reticulum communication may be a useful therapeutic target after myocardial infarction.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction

Cheng

Zheng

et al. 2021

Front. Physiol.

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“…Nowadays, 3 types of iron chelators including deferiprone, deferoxamine, and deferasirox are applied in clinical practice, mostly for the treatment of IOC (Pennell et al, 2013). Compared to the other two iron chelators, deferiprone targets hemorrhage-derived iron in IRI, which exerts a cardioprotective effect in acute MI by alleviating intramyocardial hemorrhage and cardiac hypertrophy (Behrouzi et al, 2020). Moreover, several retrospective studies revealed that deferiprone monotherapy showed better protection in heart than deferoxamine therapy or subcutaneous desferrioxamine therapy (Galanello et al, 2006;Pepe et al, 2011;Bilgin et al, 2020;Li et al, 2021).…”

Section: The Application Of Ferroptosis In Treatment Of Cvdsmentioning

confidence: 99%

Targeting Ferroptosis to Treat Cardiovascular Diseases: A New Continent to Be Explored

Huang

Yang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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Cardiovascular diseases, including cardiomyopathy, myocardial infarction, myocardial ischemia/reperfusion injury, heart failure, vascular injury, stroke, and arrhythmia, are correlated with cardiac and vascular cell death. Ferroptosis is a novel form of non-apoptotic regulated cell death which is characterized by an iron-driven accumulation of lethal lipid hydroperoxides. The initiation and execution of ferroptosis are under the control of several mechanisms, including iron metabolism, glutamine metabolism, and lipid peroxidation. Recently, emerging evidence has demonstrated that ferroptosis can play an essential role in the development of various cardiovascular diseases. Recent researches have shown the ferroptosis inhibitors, iron chelators, genetic manipulations, and antioxidants can alleviate myocardial injury by blocking ferroptosis pathway. In this review, we systematically described the mechanisms of ferroptosis and discussed the role of ferroptosis as a novel therapeutic strategy in the treatment of cardiovascular diseases.

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“…How basic research results should be applied in a clinical situation also needs further exploration. Nevertheless, inhibition of ferroptosis is thought to be a potential therapeutic option for CVDs (22,120).…”

Section: Conclusion and Perspectivementioning

confidence: 99%

The Link Between Ferroptosis and Cardiovascular Diseases: A Novel Target for Treatment

Chen

Jing

et al. 2021

Front. Cardiovasc. Med.

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Ferroptosis is an iron-dependent cell death, which is characterized by iron overload and lipid peroxidation. Ferroptosis is distinct from apoptosis, necroptosis, autophagy, and other types of cell death in morphology and function. Ferroptosis is regulated by a variety of factors and controlled by several mechanisms, including mitochondrial activity and metabolism of iron, lipid, and amino acids. Accumulating evidence shows that ferroptosis is closely related to a majority of cardiovascular diseases (CVDs), including cardiomyopathy, myocardial infarction, ischemia/reperfusion injury, heart failure, and atherosclerosis. This review summarizes the current status of ferroptosis and discusses ferroptosis as a potential therapeutic target for CVDs.

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Action of iron chelator on intramyocardial hemorrhage and cardiac remodeling following acute myocardial infarction

Cited by 40 publications

References 84 publications

RETRACTED: Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction

RETRACTED: Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction

Targeting Ferroptosis to Treat Cardiovascular Diseases: A New Continent to Be Explored

The Link Between Ferroptosis and Cardiovascular Diseases: A Novel Target for Treatment

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