Plasma nuclear and mitochondrial DNA levels in acute myocardial infarction patients

Wang, Lei; Xie, Liang; Zhang, Qigao; Cai, Xiwen; Tang, Yi; Wang, Lijun; Hang, Tao; Liu, Jing; Gong, Jianbin

doi:10.1097/mca.0000000000000231

Cited by 76 publications

(61 citation statements)

References 34 publications

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“…Atherosclerosis, in which cholesterol and white blood cells accumulate in the wall of the artery, is commonly considered as a reason of MI [6]. Even though MI is considered as a minor event, it may cause sudden death or sever haemodynamic deterioration [7]. Thus, it is really urgent to explore effective therapeutic targets for treatment of MI.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

Wang

Zhang

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Myocardial infarction (MI) is a leading cause of morbidity and mortality. Here, we sought to explore the potential role and underlying mechanism of miR-145 in MI. Methods: H9c2 cells were cultured under persistent hypoxia to simulate MI. The hypoxia-induced injury was assessed on the basis of cell viability, migration, invasion and apoptosis. The expression of miR-145 was evaluated by qRT-PCR and the influence of aberrantly expressed miR-145 on H9c2 cells under hypoxia was also estimated. Utilizing bioinformatics methods, the target genes of miR-145 were verified by luciferase reporter assay. Then, effects of abnormally expressed target gene on miR-145 silenced H9c2 cells were assessed. Finally, the phosphorylation levels of key kinases in the phosphatidylinositol-3-kinase (PI3K)/AKT and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathways were detected by Western blot analysis. Results: Hypoxia remarkably lowered viability, migration and invasion but promoted cell apoptosis. Meantime, the miR-145 level was up-regulated in H9c2 cells under hypoxia. Following experiments suggested that hypoxia-induced injury was exacerbated by miR-145 overexpression while was alleviated by miR-145 silence. Rac1 was predicted and further validated to be a target gene of miR-145. The influence of miR-145 silencing on H9c2 cells under hypoxia could be reversed by down-regulation of Rac1. Additionally, the phosphorylation levels of PI3K, AKT, MAPK and ERK were all elevated in miR-145 silenced cells and these alterations were reversed by down-regulation of Rac1. Conclusion: miR-145 silencing could protect H9c2 cells against hypoxia-induced injury by targeting Rac1, in which PI3K/AKT and MAPK/ERK pathways might be involved.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

Wang

Zhang

Wang

et al. 2017

Cell Physiol Biochem

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“…of patients following trauma (25,26), in patients with myocardial (27,28) and neurologic tissue injury (29,30), and in setting of sepsis (31,32). However, the role of mitochondria-derived DAMPs (mtDAMPs) has not been investigated in the setting of brain death, nor has their effect on allograft function been described.…”

Section: Introductionmentioning

confidence: 99%

Circulating mitochondria in deceased organ donors are associated with immune activation and early allograft dysfunction

et al. 2018

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“…Lastly, during IR injury, there is a release of mtDNA upon mitochondrial rupture, which becomes freely circulating. Given this mechanism, mtDNA has recently been considered to be a possible biomarker for myocardial infarction [7][8][9]. In addition to the apoptosis induced by mitochondrial disruption, free mtDNA can add to the cardiomyocyte death rate [10,11].…”

Section: Ischemia-reperfusion Injurymentioning

confidence: 99%

The Critical Role of Bioenergetics in Donor Cardiac Allograft Preservation

Schipper

Marsh

Ferng

et al. 2016

J. of Cardiovasc. Trans. Res.

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The traditional philosophy of ex vivo organ preservation has been to limit metabolic activity by storing organs in hypothermic, static conditions. This methodology cannot provide longevity of hearts for more than 4-6 h and is thereby insufficient to expand the number of available organs. Albeit at lower rate, the breakdown of ATP still occurs during hypothermia. Furthermore, cold static preservation does not prevent the permanent damage that occurs upon reperfusion known as ischemia-reperfusion (IR) injury. This damage is caused by increased reactive oxygen species (ROS) production in combination with mitochondrial permeability transition pore (mPTP) opening, highlighting the importance of mitochondria in ischemic storage. There has recently been a major paradigm shift in the field, with emerging research supporting changes in traditional storage approaches. Novel research suggests achieving metabolic homeostasis instead of attempting to limit metabolic activity which reduces IR injury and improves graft preservation. Maintaining high ATP levels and circumventing cold organ storage would be a much more sophisticated standard for organ storage and should be the focus of future research in organ preservation. Given the link between mPTP, Ca2(+), and ROS, managing Ca2(+) influx into the mitochondria during conditioning might be the next critical step towards preventing irreversible IR injury.

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Plasma nuclear and mitochondrial DNA levels in acute myocardial infarction patients

Cited by 76 publications

References 34 publications

MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

MicroRNA-145 Aggravates Hypoxia-Induced Injury by Targeting Rac1 in H9c2 Cells

Circulating mitochondria in deceased organ donors are associated with immune activation and early allograft dysfunction

The Critical Role of Bioenergetics in Donor Cardiac Allograft Preservation

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