Histochrome Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting Ferroptosis-Induced Cardiomyocyte Death

Hwang, Ji Won; Park, Jae-Hyun; Park, Bong‐Woo; Kim, Hyeok; Kim, Jin Ju; Sim, Woo‐Sup; Mishchenko, Natalia P.; Fedoreyev, Sergey A.; Васильева, Е. А.; Ban, Kiwon; Park, Hun‐Jun; Baek, Sang-Hong

doi:10.3390/antiox10101624

Cited by 40 publications

(29 citation statements)

References 83 publications

(119 reference statements)

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“…With the surge of results confirming the pivotal role of ferroptosis in developing heart and liver diseases, some recent studies have demonstrated how targeting the ferroptotic pathway can be beneficial in inhibiting cell death induced by iron overload. For instance, the use of both iron chelator and antioxidants have been proposed as therapeutic tools in the treatment of myocardial infarction and in preconditioning the hearts of patients undergoing reperfusion manoeuvres [ 135 ]. In liver, several physiopathological pathways can be affected by impaired iron homeostasis including alcohol-induced hepatotoxicity [ 136 ], acute liver failure [ 85 ], drug-induced liver injury [ 137 ], and hepatic fibrosis [ 138 ].…”

Section: Discussionmentioning

confidence: 99%

Iron Overload, Oxidative Stress, and Ferroptosis in the Failing Heart and Liver

et al. 2021

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Iron accumulation is a key mediator of several cytotoxic mechanisms leading to the impairment of redox homeostasis and cellular death. Iron overload is often associated with haematological diseases which require regular blood transfusion/phlebotomy, and it represents a common complication in thalassaemic patients. Major damages predominantly occur in the liver and the heart, leading to a specific form of cell death recently named ferroptosis. Different from apoptosis, necrosis, and autophagy, ferroptosis is strictly dependent on iron and reactive oxygen species, with a dysregulation of mitochondrial structure/function. Susceptibility to ferroptosis is dependent on intracellular antioxidant capacity and varies according to the different cell types. Chemotherapy-induced cardiotoxicity has been proven to be mediated predominantly by iron accumulation and ferroptosis, whereas there is evidence about the role of ferritin in protecting cardiomyocytes from ferroptosis and consequent heart failure. Another paradigmatic organ for transfusion-associated complication due to iron overload is the liver, in which the role of ferroptosis is yet to be elucidated. Some studies report a role of ferroptosis in the initiation of hepatic inflammation processes while others provide evidence about an involvement in several pathologies including immune-related hepatitis and acute liver failure. In this manuscript, we aim to review the literature to address putative common features between the response to ferroptosis in the heart and liver. A better comprehension of (dys)similarities is pivotal for the development of future therapeutic strategies that can be designed to specifically target this type of cell death in an attempt to minimize iron-overload effects in specific organs.

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Section: Discussionmentioning

confidence: 99%

Iron Overload, Oxidative Stress, and Ferroptosis in the Failing Heart and Liver

et al. 2021

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“…The hearts of rats administered early intravenous injections of HC before reperfusion exhibited remarkably reduced cardiac fibrosis and increased capillary density. By inducing the expression of NRF2 and antioxidant genes, HC can reduce cytoplasmic and mitochondrial ROS, maintain intracellular GSH levels, and enhance GPX4 activity [ 75 ]. Wang et al demonstrated that myocardial infarction was substantially reduced by dexmedetomidine (Dex), and heart function improved, along with diminished lipid peroxidation and Fe 2+ accumulation.…”

Section: Mechanisms and Targeted Therapies For Ferroptosis In Irimentioning

confidence: 99%

Ferroptosis—A New Dawn in the Treatment of Organ Ischemia–Reperfusion Injury

Zhou

Han

Guo

et al. 2022

Cells

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Ischemia–reperfusion (I/R) is a common pathological phenomenon that occurs in numerous organs and diseases. It generally results from secondary damage caused by the recovery of blood flow and reoxygenation, followed by ischemia of organ tissues, which is often accompanied by severe cellular damage and death. Currently, effective treatments for I/R injury (IRI) are limited. Ferroptosis, a new type of regulated cell death (RCD), is characterized by iron overload and iron-dependent lipid peroxidation. Mounting evidence has indicated a close relationship between ferroptosis and IRI. Ferroptosis plays a significantly detrimental role in the progression of IRI, and targeting ferroptosis may be a promising approach for treatment of IRI. Considering the substantial progress made in the study of ferroptosis in IRI, in this review, we summarize the pathological mechanisms and therapeutic targets of ferroptosis in IRI.

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“…Nevertheless, it also causes further myocardial damage ( Virani et al, 2020 ; Ren et al, 2021 ). MIRI is characterized by metabolic disturbance, cardiac dysfunction, inflammatory reaction, and cell death (apoptosis, autophagy, necrocytosis, pyroptosis, ferroptosis) ( Moens et al, 2005 ; Eltzschig and Eckle, 2011 ; Hwang et al, 2021 ; Lv et al, 2021 ; Peng et al, 2021 ).…”

Section: Myocardial Cell Apoptosis In Myocardial Ischemia/reperfusion...mentioning

confidence: 99%

Inhibition of Myocardial Cell Apoptosis Is Important Mechanism for Ginsenoside in the Limitation of Myocardial Ischemia/Reperfusion Injury

Chen

et al. 2022

Front. Pharmacol.

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Ischemic heart disease has a high mortality, and the recommended therapy is reperfusion. Nevertheless, the restoration of blood flow to ischemic tissue leads to further damage, namely, myocardial ischemia/reperfusion injury (MIRI). Apoptosis is an essential pathogenic factor in MIRI, and ginsenosides are effective in inhibiting apoptosis and alleviating MIRI. Here, we reviewed published studies on the anti-apoptotic effects of ginsenosides and their mechanisms of action in improving MIRI. Each ginsenoside can regulate multiple pathways to protect the myocardium. Overall, the involved apoptotic pathways include the death receptor signaling pathway, mitochondria signaling pathway, PI3K/Akt signaling pathway, NF-κB signaling pathway, and MAPK signaling pathway. Ginsenosides, with diverse chemical structures, regulate different apoptotic pathways to relieve MIRI. Summarizing the effects and mechanisms of ginsenosides contributes to further mechanism research studies and structure–function relationship research studies, which can help the development of new drugs. Therefore, we expect that this review will highlight the importance of ginsenosides in improving MIRI via anti-apoptosis and provide references and suggestions for further research in this field.

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Histochrome Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting Ferroptosis-Induced Cardiomyocyte Death

Cited by 40 publications

References 83 publications

Iron Overload, Oxidative Stress, and Ferroptosis in the Failing Heart and Liver

Iron Overload, Oxidative Stress, and Ferroptosis in the Failing Heart and Liver

Ferroptosis—A New Dawn in the Treatment of Organ Ischemia–Reperfusion Injury

Inhibition of Myocardial Cell Apoptosis Is Important Mechanism for Ginsenoside in the Limitation of Myocardial Ischemia/Reperfusion Injury

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