Hat der Patient einen Herzinfarkt?

Zeymer, Uwe

doi:10.1007/s15006-019-0223-3

Cited by 28 publications

(8 citation statements)

References 2 publications

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“…As a serious cardiovascular disease (CVD), myocardial infarction (MI) usually has an acute onset and high mortality, which brings a huge burden to patients and their families 1 . Although coronary intervention can reconstruct coronary blood flow after MI, ischemia reperfusion injury caused by blood flow reconstruction can also damage cardiomyocytes, leading to cardiomyocyte death 2 .…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Phenylacetyl glutamine (PAGln) enhances cardiomyocyte death after myocardial infarction through β1 adrenergic receptor

Xu,

Yang,

Wang

et al. 2023

Environmental Toxicology

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This study aims to explore the roles of phenylacetyl glutamine (PAGln) on myocardial infarction (MI) pathogenesis. Here, using targeted metabolomics analysis, it was found that the plasma metabolite PAGln was upregulated in coronary artery disease (CAD) patients and MI mice and could be an independent risk factor for CAD. In vivo and in vitro functional experiments revealed that PAGln pretreatment enhanced MI‐induced myocardial injury and cardiac fibrosis, as evident by the increased infarct size, cardiomyocyte death, and the upregulated expression of cardiac fibrosis markers (Col1a1 and α‐SMA). Combined with RNA‐sequencing analysis and G protein‐coupled receptor (GPCR) inhibitor, we found that the GPCR signaling activation is essential for PAGln‐mediated effects on cardiomyocyte death. Furthermore, drug affinity responsive target stability and cellular thermal shift assay demonstrated that PAGln could interact with β1‐adrenergic receptor (AR). Moreover, β1‐AR blocker treatment indeed extended the cardiac remodeling after PAGln‐enhanced MI. These results suggest that PAGln might be a potential therapeutic target for extending the cardiac remodeling window in MI patients that signals via β1‐AR.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Phenylacetyl glutamine (PAGln) enhances cardiomyocyte death after myocardial infarction through β1 adrenergic receptor

Xu,

Yang,

Wang

et al. 2023

Environmental Toxicology

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“…Acute myocardial infarction is a common heart disease. In the process of treatment, the myocardial blood supply in the ischemic area should be restored as soon as possible, which is of great significance to improve the prognosis [ 23 , 24 ]. The proliferation and neovascularization of myocardial cell are two major biological processes of AMI cardiac repair.…”

Section: Discussionmentioning

confidence: 99%

Regulatory Mechanism of circEIF4G2 Targeting miR-26a in Acute Myocardial Infarction

Zhang

Long

et al. 2022

Journal of Healthcare Engineering

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Background. Acute myocardial infarction (AMI) involves a series of complex cellular and molecular events, including circular RNAs (circRNAs), microRNAs (miRNAs) and other noncoding RNAs. Objective. In this study, the regulation mechanism of circEIF4G2 acting on miR-26a on HUVECs (Human Umbilical Vein Endothelial Cells) proliferation, cell cycle and angiogenesis ability was mainly explored in the vascular endothelial growth factor induced (VEGF-induced) angiogenesis model. Methods. VEGF induced HUVECs angiogenesis model was constructed, and the expression of circEIF4G2 and miR-26a in VEGF model was detected by qRT-PCR. When circEIF4G2 and miR-26a were knocked down or overexpressed in HUVECs, qRT-PCR was used to detect the expression of circEIF4G2 and miR-26a, CCK-8 was used to detect cell proliferation, flow cytometry was used to detect the cell cycle transition of HUVECs, and cell formation experiment was used to detect the ability of angiogenesis. MiRanda database and Targetscan predicted the binding site of circEIF4G2 and miR-26a, lucifase reporting assay and RNA pull down assay verified the interaction between circEIF4G2 and miR-26a. Results. After HUVECs were treated with VEGF, circEIF4G2 was significantly upregulated. After circEIF4G2 was knocked down, the proliferation and angiogenesis of HUVECs cells were decreased, and the process of cell cycle G0/G1 phase was blocked. The overexpression of miR-26a reduced the proliferation and angiogenesis of HUVECs cells and blocked the cell cycle progression of G0/G1 phase. Double lucifase reporter gene assay verified that circEIF4G2 could directly interact with miR-26a through the binding site, and RNA Pull down assay further verified the interaction between circEIF4G2 and miR-26a. When circEIF4G2 and miR-26a were knocked down simultaneously in HUVECs, it was found that knocking down miR-26a could reverse the inhibition of circEIF4G2 on cell proliferation, cycle and angiogenesis. Conclusion. In the VEGF model, circEIF4G2 was highly expressed and miR-26a was low expressed. MiR-26a regulates HUVECs proliferation, cycle and angiogenesis by targeting circEIF4G2.

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“…3,4 Recently, large numbers of studies have clearly pointed out that myocardial inflammation after MI, extracellular matrix damage and myocardial repair after MI exert an extremely vital influence on the occurrence of cardiac rupture. 5,6 We wondered about the molecular mechanism of cardiomyocyte apoptosis and myocardial inflammation underlying MI.…”

Section: Introductionmentioning

confidence: 99%

LINC00936 exacerbated myocardial infarction progression via miR-4795-3p/Wnt3a signaling pathway based on biological and imaging methods

Wang

2022

Perfusion

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Objective LncRNAs show great potential in diagnosing and treating myocardial infarction (MI). Clarifying the mechanism of lncRNAs on MI is of great significance for the application of MI biomarkers. Therefore, this report intended to determine the role and mechanism of LINC00936 on MI by biological and imaging methods. Methods Hypoxia H9C2 model was established by hypoxia treatment. Flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assay detected the apoptosis of H9C2. H2DCFDA staining and enzyme-linked immunosorbent assay (ELISA) was used to detect the reactive oxygen species (ROS) accumulation and Lactate dehydrogenase (LDH) contents, respectively. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect LINC00936, Wnt3a and miR-4795-3p levels. Western blot detected Wnt3a protein expression. Dual luciferase reporter assays detected the relationship of miR-4795-3p to LINC00936 or Wnt3a. Echocardiography analysis detected cardiac function. 2,3,5-Triphenyltetrazolium chloride (TTC) detected the infarct size. Masson staining detected the pathological changes. Results LINC00936 level was elevated in the MI patients compared with the controls. Overexpression of LINC00936 promoted apoptosis and ROS accumulation in hypoxia H9C2 model and exacerbated MI progression in vivo. miR-4795-3p bound with LINC00936 in H9C2 cells and miR-4795-3p mimics inhibited apoptosis and ROS accumulation in hypoxia H9C2 model regulated by LINC00936. Wnt3a was targeted by miR-4795-3p and Wnt3a elevation promoted apoptosis and ROS accumulation in hypoxia H9C2 model. Conclusion In this report, we illustrated that LINC00936 exacerbated MI progression via the miR-4795-3p/Wnt3a signaling pathway based on biological and imaging methods. These findings might provide potential molecular target for the diagnosis and treatment of MI.

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Hat der Patient einen Herzinfarkt?

Cited by 28 publications

References 2 publications

RETRACTED: Phenylacetyl glutamine (PAGln) enhances cardiomyocyte death after myocardial infarction through β1 adrenergic receptor

RETRACTED: Phenylacetyl glutamine (PAGln) enhances cardiomyocyte death after myocardial infarction through β1 adrenergic receptor

Regulatory Mechanism of circEIF4G2 Targeting miR-26a in Acute Myocardial Infarction

LINC00936 exacerbated myocardial infarction progression via miR-4795-3p/Wnt3a signaling pathway based on biological and imaging methods

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