Filtered By:
Condition: Heart Attack

This page shows you your search results in order of date. This is page number 13.

Order by Relevance | Date

Total 280 results found since Jan 2013.

Betulinic acid alleviates myocardial hypoxia/reoxygenation injury via inducing Nrf2/HO-1 and inhibiting p38 and JNK pathways.
Abstract Myocardial ischemia reperfusion injury (I/RI) can lead to acute myocardial infarction (MI), which is a common cardiovascular disease (CVD) leading to morbidity and mortality worldwide. Betulinic acid exerts protective effect on myocardial I/RI in rats; however, the mechanism remains unknown. The aim of the current study was to evaluate the effect of betulinic acid on myocardial I/RI in vitro and further investigate the underlying mechanism. Our results showed that betulinic acid increased cell viability and decreased lactate dehydrogenase (LDH) release in H9c2 cells exposed to H/R. Betulinic acid was foun...
Source: European Journal of Pharmacology - August 17, 2018 Category: Drugs & Pharmacology Authors: Wang D, Chen T, Liu F Tags: Eur J Pharmacol Source Type: research

Dysregulation of CD69 by overexpression of microRNA ‑367‑3p associated with post‑myocardial infarction cardiac fibrosis.
In conclusion, these results provide evidence that a decrease in miR‑367‑3p levels may be associated with cardiac fibrosis. PMID: 30015935 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - July 18, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Rac1 promotes the survival of H9c2 cells during serum deficiency targeting JNK/c-JUN/Cyclin-D1 and AKT2/MCL1 pathways.
Authors: Zhao J, Jie Q, Li G, Li Y, Liu B, Li H, Luo J, Qin X, Li Z, Wei Y Abstract Rac1, known as a "molecular switch", plays a crucial role in plenty of cellular processes. Rac1 aggravates the damage of myocardial cells in the process of myocardial ischemia-reperfusion during myocardial infarction through activating the NADPH oxidase and bringing about the reactive oxygen species(ROS) generation. Myocardial ischemia and hypoxia are the basic pathogenesis of myocardial infarction and the underlying mechanisms are intricate and varied. Moreover, the regulatory effect of Rac1 on myocardial cells in the condition of ...
Source: International Journal of Medical Sciences - July 18, 2018 Category: Biomedical Science Tags: Int J Med Sci Source Type: research

Heat-shock transcription factor 1 is critically involved in the ischaemia-induced cardiac hypertrophy via JAK2/STAT3 pathway.
Abstract Cardiac hypertrophy after myocardial infarction (MI) is an independent risk factor for heart failure. Regression of cardiac hypertrophy has emerged as a promising strategy in the treatment of MI patients. Here, we have been suggested that heat-shock transcription factor 1 (HSF1) is a novel repressor of ischaemia-induced cardiac hypertrophy. Ligation of left anterior descending coronary was used to produce MI in HSF1-deficient heterozygote (KO), HSF1 transgenic (TG) mice and their wild-type (WT) littermates, respectively. Neonatal rat cardiomyocytes (NRCMs) were treated by hypoxia to mimic MI in vitro. The...
Source: J Cell Mol Med - July 11, 2018 Category: Molecular Biology Authors: Yuan L, Qiu L, Ye Y, Wu J, Wang S, Wang X, Zhou N, Zou Y Tags: J Cell Mol Med Source Type: research

Thymoquinone Attenuates Myocardial Ischemia/Reperfusion Injury Through Activation of SIRT1 Signaling
Conclusions: The findings in this study demonstrate that TQ is efficient in attenuating MI/R injury through activation of the SIRT1 signaling pathway, which can thus reduce mitochondrial oxidative stress damage and cardiomyocyte apoptosis.Cell Physiol Biochem 2018;47:1193 –1206
Source: Cellular Physiology and Biochemistry - June 18, 2018 Category: Cytology Source Type: research

Long Noncoding RNA (lncRNA) n379519 Promotes Cardiac Fibrosis in Post-Infarct Myocardium by Targeting miR-30.
CONCLUSIONS These findings reveal a novel function of n379519-miR-30 axis as a negative regulator for the treatment of MI-induced cardiac fibrosis and the associated cardiac dysfunction. PMID: 29889825 [PubMed - in process]
Source: Medical Science Monitor - June 13, 2018 Category: Research Tags: Med Sci Monit Source Type: research

Inhibition of miR-135b by SP-1 promotes hypoxia-induced vascular endothelial cell injury via HIF-1 α.
In conclusion, the SP-1/miR-135b/HIF-1α axis may play a critical role in hypoxia-induced vascular endothelial injury. Our study thus provides novel insights into the role of this transcription factor and miRNAs in the pathogenesis of hypoxia-induced cardiac dysfunctions. PMID: 29883713 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - June 5, 2018 Category: Cytology Authors: Yang S, Yin J, Hou X Tags: Exp Cell Res Source Type: research

miR-21 promotes cardiac fibroblast-to-myofibroblast transformation and myocardial fibrosis by targeting Jagged1.
This study aimed to investigate the role of miR-21 in the regulation of CMT and myocardial fibrosis. Primary rat CFs were isolated from young SD rats and treated with TGF-β1, miR-21 sponge or Jagged1 siRNA. Cell proliferation, invasion and adhesion were detected. MI model was established in male SD rats using LAD ligation method and infected with recombinant adenovirus. The heart function and morphology was evaluated by ultrasonic and histological analysis. We found that TGF-β1 induced the up-regulation of miR-21 and down-regulation of Jagged1 in rat CFs. Luciferase assay showed that miR-21 targeted 3'-UTR of Jagged1 in ...
Source: J Cell Mol Med - May 28, 2018 Category: Molecular Biology Authors: Zhou XL, Xu H, Liu ZB, Wu QC, Zhu RR, Liu JC Tags: J Cell Mol Med Source Type: research

Integrin β3 inhibits hypoxia-induced apoptosis in cardiomyocytes.
Abstract Hypoxia-induced apoptosis plays an important role in cardiovascular diseases. Integrin β3 is one of the main integrin heterodimer receptors on the surface of cardiac myocytes. However, despite the important role that integrin β3 plays in the cardiovascular disease, its exact role in the hypoxia response remains unclear. Hence, in the present investigation we aimed to study the role of integrin β3 in hypoxia-induced apoptosis in H9C2 cells and primary rat myocardial cells. MTT assay, flow cytometry and TUNEL assay results showed that hypoxia inhibited cardiomyocyte proliferation and induced cardiomyocyt...
Source: Acta Biochimica et Biophysica Sinica - May 23, 2018 Category: Biochemistry Authors: Su Y, Tian H, Wei L, Fu G, Sun T Tags: Acta Biochim Biophys Sin (Shanghai) Source Type: research

MicroRNA ‑20b‑5p promotes ventricular remodeling by targeting the TGF‑β/Smad signaling pathway in a rat model of ischemia‑reperfusion injury.
MicroRNA‑20b‑5p promotes ventricular remodeling by targeting the TGF‑β/Smad signaling pathway in a rat model of ischemia‑reperfusion injury. Int J Mol Med. 2018 May 18;: Authors: Liang ZG, Yao H, Xie RS, Gong CL, Tian Y Abstract Myocardial ischemic injury results from severe impairment of the coronary blood supply and may lead to metabolic and ultrastructural changes, thereby causing irreversible damage. MicroRNA (miR)‑20b‑5p has been demonstrated to be involved in malignancies of the breast, colorectum, stomach, blood and oropharynx. The present study aimed to investigate the effects of ...
Source: International Journal of Molecular Medicine - May 18, 2018 Category: Molecular Biology Authors: Liang ZG, Yao H, Xie RS, Gong CL, Tian Y Tags: Int J Mol Med Source Type: research

MiR-1908 improves cardiac fibrosis after myocardial infarction by targeting TGF- β1.
CONCLUSIONS: MiR-1908 can improve the myocardial fibrosis through the target gene TGF-β1. PMID: 29687863 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - April 26, 2018 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Suppression of lncR-30245 alleviates myocardial infarction induced cardiac fibrosis via the PPAR- γ/CTGF pathway
Conclusion Our study indicates that the lncR-30245/PPAR-γ/CTGF pathway mediates MI-induced cardiac fibrosis and might be a therapeutic target for various cardiac diseases associated with fibrosis. Teaser LncR-30245, a conserved lncRNA promotes collagen production and cardiac fibroblast proliferation. Knockdown of lncR-30245 significantly inhibits TGF-β1-induced collagen production and cardiac fibroblast proliferation. Importantly, silencing of lncR-30245 significantly alleviates cardiac fibrosis and improves cardiac function after MI. The PPAR-γ/CTGF signaling pathway is involved in the regulation of cardiac fibrosis by...
Source: Canadian Journal of Cardiology - April 19, 2018 Category: Cardiology Source Type: research

The Protective Effect of Total Flavones from Rhododendron simsii Planch. on Myocardial Ischemia/Reperfusion Injury and Its Underlying Mechanism.
Conclusions: The results indicate that the protective effect of TFR on I/R injury may be correlated with its blocking UTR and the subsequent inhibition of RhoA/ROCK signaling pathway. PMID: 29541143 [PubMed]
Source: Evidence-based Complementary and Alternative Medicine - March 17, 2018 Category: Complementary Medicine Tags: Evid Based Complement Alternat Med Source Type: research

PEDF improves cardiac function in rats subjected to myocardial ischemia/reperfusion injury by inhibiting ROS generation via PEDF ‑R.
PEDF improves cardiac function in rats subjected to myocardial ischemia/reperfusion injury by inhibiting ROS generation via PEDF‑R. Int J Mol Med. 2018 Mar 09;: Authors: Zhao Q, Liu Z, Huang B, Yuan Y, Liu X, Zhang H, Qiu F, Zhang Y, Li Y, Miao H, Dong H, Zhang Z Abstract The prevention and management of myocardial ischemia/reperfusion (MI/R) injury is an essential part of coronary heart disease surgery and is becoming a major clinical problem in the treatment of ischemic heart disease. Previous studies by our group have demonstrated that pigment epithelium‑derived factor (PEDF) improves cardiac f...
Source: International Journal of Molecular Medicine - March 9, 2018 Category: Molecular Biology Authors: Zhao Q, Liu Z, Huang B, Yuan Y, Liu X, Zhang H, Qiu F, Zhang Y, Li Y, Miao H, Dong H, Zhang Z Tags: Int J Mol Med Source Type: research

Abnormal Downregulation of Caveolin-3 Mediates the Pro-Fibrotic Action of MicroRNA-22 in a Model of Myocardial Infarction
Conclusions: Our findings demonstrate that miR-22 accelerates cardiac fibrosis through the miR-22-Cav3-PKC ε pathway, which, therefore, may represent a new therapeutic target for treatment of excessive fibrosis-associated cardiac diseases.Cell Physiol Biochem 2018;45:1641 –1653
Source: Cellular Physiology and Biochemistry - February 27, 2018 Category: Cytology Source Type: research