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Condition: Heart Attack

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Total 280 results found since Jan 2013.

Silencing of ATP2B1-AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA-mediated NF- κB signalling pathway.
This study aimed to investigate the effect of long intergenic non-protein-coding RNA (lincRNA) ATPase plasma membrane Ca2+ transporting 1 antisense RNA 1 (ATP2B1-AS1) against MI by targeting nuclear factor-kappa-B inhibitor alpha (NFKBIA) and mediating the nuclear factor-kappa-B (NF-κB) signalling pathway. An MI mouse model was established and idenepsied by cardiac function evaluation. It was determined that ATP2B1-AS1 was highly expressed, while NFKBIA was poorly expressed and NF-κB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1-AS1 vecto...
Source: J Cell Mol Med - March 9, 2020 Category: Molecular Biology Authors: Song KY, Zhang XZ, Li F, Ji QR Tags: J Cell Mol Med Source Type: research

(-)-Epigallocatechin Gallate Promotes MicroRNA 145 Expression against Myocardial Hypoxic Injury through Dab2/Wnt3a/ β-catenin.
This study demonstrated that EGCG increased miR-145, Wnt3a, and β-catenin expression but attenuated Dab2 expression. Moreover, EGCG ameliorated myocardial ischemia in vivo. The novel suppressive effect was mediated through the miR-145 and Dab2/Wnt3a/β-catenin pathways. PMID: 32138537 [PubMed - as supplied by publisher]
Source: The American Journal of Chinese Medicine - March 4, 2020 Category: Complementary Medicine Authors: Lin CM, Fang WJ, Wang BW, Pan CM, Chua SK, Hou SW, Shyu KG Tags: Am J Chin Med Source Type: research

Secretome Analysis of Cardiomyocytes Identifies PCSK6 as a Novel Player in Cardiac Remodeling After Myocardial Infarction.
Conclusions: A novel mass spectrometry-based approach allows the investigation of the secretome of primary cardiomyocytes. Analysis of hypoxia-induced secretion led to the identification of PCSK6 to be crucially involved in cardiac remodeling after acute myocardial infarction. PMID: 32100557 [PubMed - as supplied by publisher]
Source: Circulation - February 25, 2020 Category: Cardiology Authors: Kuhn TC, Knobel J, Burkert-Rettenmaier S, Li X, Meyer IS, Jungmann A, Sicklinger F, Backs J, Lasitschka F, Müller OJ, Katus HA, Krijgsveld J, Leuschner F Tags: Circulation Source Type: research

GSE145697 The role of lncRNA Sarrah in human cardiomyocytes
Contributors : Reinier A Boon ; D J TrembinskiSeries Type : Expression profiling by arrayOrganism : Homo sapiensLong non-coding RNAs (lncRNAs) contribute to (patho)physiological processes in the heart. Aging is the major risk factor for cardiovascular disease and cardiomyocyte apoptosis is an underlying cause for age-related cardiac dysfunction. RNA sequencing of cardiomyocytes from young and aged mouse hearts revealed several aging-regulated lncRNAs. An siRNA screen for caspase activity identified the aging-regulated lncRNA Sarrah (ENSMUST00000140003) as anti-apoptotic, which we confirmed in human cells (human SARRAH is a...
Source: GEO: Gene Expression Omnibus - February 22, 2020 Category: Genetics & Stem Cells Tags: Expression profiling by array Homo sapiens Source Type: research

Glatiramer acetate protects against oxygen-glucose deprivation/reperfusion-induced injury by inhibiting Egr-1 in H9c2 cells
Publication date: April 2020Source: Molecular Immunology, Volume 120Author(s): Jian Du, Wei Lv, Sitong Yang, Jia Liu, Juan Zhen, Jiyan LengAbstractMyocardial infarction (MI) or heart attack is a deadly event with high prevalence. In the present study, we investigated the effects of the polypeptide copolymer glatiramer acetate (GA) in H9c2 rat cardiomyocytes exposed to oxygen-glucose deprivation/reperfusion injury. Immediately following MI, an acute inflammatory response is triggered that causes activation of various proinflammatory cytokines, infiltration of immune cells, and neovascularization. This response is largely me...
Source: Molecular Immunology - February 18, 2020 Category: Allergy & Immunology Source Type: research

CircRNA 010567 improves myocardial infarction rats through inhibiting TGF- β1.
CONCLUSIONS: CircRNA 010567 siRNA can improve the cardiac function, alleviate the MF, and inhibit the myocardial apoptosis, thereby further suppressing MI-induced MF, whose mechanism may be related to the inhibition on the TGF-β1 signaling pathway. PMID: 31957851 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - January 21, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Tongxinluo Attenuates Myocardiac Fibrosis after Acute Myocardial Infarction in Rats via Inhibition of Endothelial-to-Mesenchymal Transition.
In conclusion, TXL attenuates MF after AMI by inhibiting EndMT and through activating the NRG-1/ErbB- PI3K/AKT signalling cascade. PMID: 31317035 [PubMed - indexed for MEDLINE]
Source: Biomed Res - December 21, 2019 Category: Research Authors: Yin Y, Zhang Q, Zhao Q, Ding G, Wei C, Chang L, Li H, Bei H, Wang H, Liang J, Jia Z Tags: Biomed Res Int Source Type: research

LncRNA TUG1 mediates ischemic myocardial injury by targeting miR-132-3p/HDAC3 axis.
CONCLUSIONS: The TUG1/miR-132-3p/HDAC3 axis critically regulates ROS production and the pathogenic development of AMI. Targeting TUG1, up-regulating miR-132-3p, or inhibiting HDAC3 may benefit AMI treatment. PMID: 31858814 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Heart and Circulatory Physiology - December 19, 2019 Category: Physiology Authors: Su Q, Liu Y, Lv XW, Dai RX, Yang XH, Kong BH Tags: Am J Physiol Heart Circ Physiol Source Type: research

LncRNA MALAT1 knockdown alleviates myocardial apoptosis in rats with myocardial ischemia-reperfusion through activating PI3K/AKT signaling pathway.
CONCLUSIONS: The MALAT1 knockdown can markedly improve the I/R-induced myocardial injury and promote the cardiac function of rats, whose mechanism may be related to the activation of the AKT signaling pathway by MALAT1 siRNA. Therefore, lncRNA MALAT1 is expected to be a new therapeutic target for myocardial I/R injury. PMID: 31841208 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - December 18, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Effects of lncRNA MALAT1-mediated β-catenin signaling pathway on myocardial cell apoptosis in rats with myocardial ischemia/reperfusion injury.
CONCLUSIONS: MALAT1 knockdown can significantly ameliorate the I/R-induced myocardial injury and improve the cardiac function of the rats, whose mechanism is probably correlated with the inhibition of MALAT1 siRNA on β-catenin. Therefore, MALAT1 siRNA is expected to become a new target for the treatment of myocardial infarction. PMID: 31773707 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - November 28, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Effect of lncRNA GAS5 on rats with acute myocardial infarction through regulating miR-21.
CONCLUSIONS: SiRNA GAS5 can enhance the cardiac function of AMI model rats, relieve pathological damage, reduce myocardial cell apoptosis, and inhibit the occurrence of myocardial fibrosis. The possible underlying mechanism may be associated with up-regulation of miR-21. PMID: 31646590 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - October 26, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Silence of lncRNA XIST represses myocardial cell apoptosis in rats with acute myocardial infarction through regulating miR-449.
CONCLUSIONS: Knockdown of lncRNA XIST can repress the myocardial cell apoptosis in AMI model rats by downregulating miR-449 level. PMID: 31646589 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - October 26, 2019 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Deletion of Neuropeptide Y Attenuates Cardiac Dysfunction and Apoptosis During Acute Myocardial Infarction
Increasing neuropeptide Y (NPY) has been shown to be a risk factor for cardiovascular diseases. However, its role and mechanism in myocardial infarction (MI) have not yet been fully understood. H9c2 cells and neonatal rat ventricular myocytes with loss of function of NPY and rats with global knockout were used in this study. MI model of rats was induced by the ligation of left coronary artery, and the extent of MI was analyzed through echocardiographic, pathological, and molecular analyses. Our data demonstrated that NPY expression was significantly increased in MI rats and hypoxia/hydrogen peroxide (H2O2)-treated cardiomy...
Source: Frontiers in Pharmacology - October 23, 2019 Category: Drugs & Pharmacology Source Type: research

PHLPP2 downregulation protects cardiomyocytes against hypoxia-induced injury through reinforcing Nrf2/ARE antioxidant signaling
Publication date: Available online 11 October 2019Source: Chemico-Biological InteractionsAuthor(s): Aiping Jin, Bing Li, Wei Li, Dan XiaoAbstractCardiomyocyte injury induced by acute myocardial infarction contributes to myocardial dysfunction. Accumulating evidence has demonstrated that pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2) is a cytoprotective protein that protects against various adverse injuries. However, whether PHLPP2 participates in regulating myocardial-infarction-induced cardiomyocyte injury remains unknown. In the present study, we aimed to investigate the biological role and...
Source: Chemico Biological Interactions - October 12, 2019 Category: Biochemistry Source Type: research

PHLPP2 downregulation protects cardiomyocytes against hypoxia-induced injury through reinforcing Nrf2/ARE antioxidant signaling.
Abstract Cardiomyocyte injury induced by acute myocardial infarction contributes to myocardial dysfunction. Accumulating evidence has demonstrated that pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2) is a cytoprotective protein that protects against various adverse injuries. However, whether PHLPP2 participates in regulating myocardial-infarction-induced cardiomyocyte injury remains unknown. In the present study, we aimed to investigate the biological role and molecular mechanism of PHLPP2 in regulating hypoxia-induced cardiomyocyte injury. Cardiomyocytes were cultured in an anaerobic...
Source: Chemico-Biological Interactions - October 10, 2019 Category: Molecular Biology Authors: Jin A, Li B, Li W, Xiao D Tags: Chem Biol Interact Source Type: research