Advanced research on the regulated necrosis mechanism in myocardial ischemia-reperfusion injury

Deng, Jianying

doi:10.1016/j.ijcard.2021.04.042

Cited by 12 publications

(8 citation statements)

References 50 publications

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“…e pathophysiological mechanism of myocardial ischemia-reperfusion injury is complex. Studies have shown that myocardial ischemia can promote in ammation and oxidative stress translation and can lead to myocardial apoptosis through reperfusion, in which inammatory factors can activate and chemotaxis leukocytes, which are also the products of activation of the leukocytes, which can aggravate myocardial injury [1,[7][8][9]. Superoxide dismutase (SOD) is essential to prevent oxidative stress, and it can e ectively resist the damage of oxygen free radicals to the body through its antioxidant and antifree radical functions [10].…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Sun

Tan

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Myocardial ischemia/reperfusion (MIR) injury contributes to the exacerbation of heart disease by causing cardiac arrhythmias, myocardial infarction, and even sudden death. Studies have found that paeoniflorin (PF) has a protective effect on coronary artery disease (CAD). However, the mechanism of PF in MIR has not been fully investigated. The purpose of this study was to investigate the functional role of PF in H9c2 cells subjected to hypoxia/reoxygenation (H/R). Here, PF treatment enhanced cell viability in H/R-stimulated H9c2 cells. In H9c2 cells, PF treatment reduced the formation of reactive oxygen species (ROS) induced by H/R. In H/R-stimulated H9c2 cells, PF also increased the activity of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase. Furthermore, PF protected H9c2 cells against H/R-induced apoptosis, as demonstrated by increased Bcl-2 expression, decreased Bax expression, and decreased caspase-3 activity. Furthermore, PF increased the levels of p-AMPK and nuclear Nrf2 expression in response to H/R stimulation. AMPK inhibition, on the other hand, abolished the PF-mediated increase in Nrf2 signaling and the cardiac-protective effect in H9c2 cells exposed to H/R. These data suggest that PF protected H9c2 cells against H/R-induced oxidative stress and apoptosis through modulating the AMPK/Nrf2 signaling pathway. Our findings support the therapeutic potential of PF in myocardial I/R damage.

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Section: Introductionmentioning

confidence: 99%

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Sun

Tan

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…28 The aforementioned nine programs participate in complex mechanisms underlying the death of cardiomyocytes. 29,30 Among these, ferroptosis is considered a contributor to I/R injury;…”

Section: Discussionmentioning

confidence: 99%

“…These cell death programs, particularly the regulated forms of cardiomyocyte death, play significant roles in major cardiac syndromes such as MI with reperfusion and heart failure 28 . The aforementioned nine programs participate in complex mechanisms underlying the death of cardiomyocytes 29,30 . Among these, ferroptosis is considered a contributor to I/R injury; hence, targeting ferroptosis may be a promising protective therapy against I/R injury 31 .…”

Section: Discussionmentioning

confidence: 99%

Mechanism of DYRK1a in myocardial ischemia–reperfusion injury by regulating ferroptosis of cardiomyocytes

Wang,

Xu,

Cao

et al. 2023

The Kaohsiung J of Med Scie

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This study aimed to explore the role and mechanism of DYRK1a regulating ferroptosis of cardiomyocytes during myocardial ischemia–reperfusion injury (MIRI). H9c2 cells treated with oxygen–glucose deprivation/reoxygenation (OGD/R) were used as MIRI cell models and transfected with sh‐DYRK1a or/and erastin. Cell viability, apoptosis, and DYRK1a mRNA/protein expression were measured accordingly. The levels of reactive oxygen species (ROS), iron, malondialdehyde (MDA), and glutathione (GSH) were determined. The expression of ferroptosis‐related proteins (GPX4, SLC7A11, ACSL4, and TFR1) was detected using western blotting. The MIRI rat model was established to explore the possible role of DYRK1a suppression in cell injury and ferroptosis. OGD/R cells showed elevated mRNA and protein expression for DYRK1a. OGD/R cells transfected with sh‐DYRK1a showed elevated cell viability, GSH content, increased GPX4 and SLC7A11 expression, suppressed iron content, MDA, ROS, ACSL4, and TFR1 expression, and reduced apoptosis rate, whereas co‐transfection of sh‐DYRK1a with erastin reversed the attenuation of sh‐DYRK1a on MIRI. The suppressive effect of sh‐DYRK1a on MI/R injury was confirmed in an MIRI rat model. DYRK1a mediates ferroptosis of cardiomyocytes to deteriorate MIRI progression.

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“…While I/R is effective in restoring blood supply to ischemic tissue, it may also lead to additional damage, including the apoptosis and death of myocardial cells, resulting in cell loss and cardiac dysfunction [12]. Thus, it is extremely important to devise methods of preventing and treating I/R injuries.…”

Section: Discussionmentioning

confidence: 99%

MiR-19a-3p mitigates hypoxia/reoxygenation-induced apoptosis in H9C2 cardiomyocytes by targeting SOCS3

Xia

Bao

et al. 2022

Preprint

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The available treatment strategies for myocardial ischemia-reperfusion (I/R) injuries have not been so much effective. MicroRNAs (miRNAs) from the miR-19 family, which includes miR-19a and miR-19b, modulate both proliferation and apoptosis in the myocardium. The correlation between I/R injury and miR-19a-3p is unknown. Here, the role of miR-19a-3p in injuries induced by I/R was investigated in H9C2 cardiomyocytes. The MiR-19a-3p Levels were determined to be reduced after hypoxia/reoxygenation (H/R) and miR-19a-3p overexpression reduced apoptosis resulting from H/R, improving the activity of the cells. The opposite effect was observed when miR-19a-3p was inhibited. Potential miR-19a-3p targets were investigated using bioinformatics, identifying Protein Suppressor of cytokine signaling-3 (SOCS3), which was verified by luciferase reporter assays. SOCS3 levels were lower by overexpression of miR-19a-3p. SOCS3 silencing prevented apoptosis induced by miR-19a-3p inhibition, whereas overexpression of SOCS3 blocked a miR-19a-3p mimic's effects on apoptosis. According to these findings, miR-19a-3p reduces apoptosis and injury induced by H/R in cardiomyocytes through targeting SOCS3, and that targeting miR-19a-3p/SOCS3 signalling may present a new strategy in the therapy of myocardial I/R injury.

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Advanced research on the regulated necrosis mechanism in myocardial ischemia-reperfusion injury

Cited by 12 publications

References 50 publications

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Paeoniflorin Protects H9c2 Cardiomyocytes against Hypoxia/Reoxygenation Induced Injury via Regulating the AMPK/Nrf2 Signaling Pathway

Mechanism of DYRK1a in myocardial ischemia–reperfusion injury by regulating ferroptosis of cardiomyocytes

MiR-19a-3p mitigates hypoxia/reoxygenation-induced apoptosis in H9C2 cardiomyocytes by targeting SOCS3

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