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Condition: Heart Attack

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Total 12 results found since Jan 2013.

MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3.
Authors: Wang J, Chen X, Huang W Abstract Hypoxia-induced apoptosis and inflammation play an important role in cardiovascular diseases including myocardial infarction (MI). miR-369 has been suggested to be a key regulator of cardiac fibrosis. However, the role of miR-369 in regulating hypoxia-induced heart injury remains unknown. Our data indicated that miR-369 expression was significantly down-regulated and TRPV3 was significantly up-regulated in myocardial tissue after MI in rats and in hypoxic-treated neonatal rat cardiomyocytes (NRCMs). In addition, we observed that hypoxia significantly promoted apoptosis and ...
Source: Brazilian Journal of Medical and Biological Research - January 21, 2021 Category: Research Tags: Braz J Med Biol Res Source Type: research

MicroRNA-369 attenuates hypoxia-induced cardiomyocyte apoptosis and inflammation via targeting TRPV3
Braz J Med Biol Res. 2021 Jan 15;54(3):e10550. doi: 10.1590/1414-431X202010550. eCollection 2021.ABSTRACTHypoxia-induced apoptosis and inflammation play an important role in cardiovascular diseases including myocardial infarction (MI). miR-369 has been suggested to be a key regulator of cardiac fibrosis. However, the role of miR-369 in regulating hypoxia-induced heart injury remains unknown. Our data indicated that miR-369 expression was significantly down-regulated and TRPV3 was significantly up-regulated in myocardial tissue after MI in rats and in hypoxic-treated neonatal rat cardiomyocytes (NRCMs). In addition, we obse...
Source: Braz J Med Biol Res - January 20, 2021 Category: Research Authors: Jinghao Wang Xu Chen Wei Huang Source Type: research

PERK Overexpression-Mediated Nrf2/HO-1 Pathway Alleviates Hypoxia/Reoxygenation-Induced Injury in Neonatal Murine Cardiomyocytes via Improving Endoplasmic Reticulum Stress.
Abstract Reperfusion processes following acute myocardial infarction (AMI) have been reported to induce additional cardiomyocyte death, known as ischemia-reperfusion (I/R) injury. Endoplasmic reticulum (ER) stress is reported to be involved in the development of I/R injury. There is evidence that PERK exerts beneficial roles in alleviating ER stress. Here, we investigated whether upregulation of PERK improved cardiomyocytes injury induced by I/R. Specific siRNAs or adenovirus vectors were incubated with isolated neonatal cardiomyocytes (NCMs) to regulate expression levels of target genes including PERK, Nrf2, and ...
Source: Biomed Res - April 21, 2020 Category: Research Authors: Wang J, Lu L, Chen S, Xie J, Lu S, Zhou Y, Jiang H Tags: Biomed Res Int 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

MiR-138-5p exacerbates hypoxia/reperfusion-induced heart injury through the inactivation of SIRT1-PGC-1 α
ConclusionsIn conclusion, our study demonstrated that miR-138-5p could promote cardiac ischemia injury via inhibition of the silent information regulator 1 and peroxisome proliferator-initiated receptor gamma and coactivator 1 alpha (SIRT1 –PGC-1α) axis.
Source: Inflammation Research - July 15, 2019 Category: Research Source Type: research

Resveratrol protects against isoproterenol induced myocardial infarction in rats through VEGF-B/AMPK/eNOS/NO signaling pathway.
In this study, we investigated the protective effect of RSV on myocardial infarction (MI) in rats and further explored the underlying signal pathway after VEGF-B. Rats received RSV or normal saline by intragastric administration for 7 consecutive days and followed by subcutaneously isoproterenol (ISO) or normal saline injections for another 2 days. We found that RSV pretreatment prevented the unfavorable changes in HW/BW, HW/TL, infarct size and cell apoptosis in ISO treated rats. Moreover, superoxide and malondialdehyde (MDA) production were significantly reduced and superoxide dismutase (SOD) was increased by RSV in ISO...
Source: Free Radical Research - December 13, 2018 Category: Research Tags: Free Radic Res 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

P2X7 receptor regulates sympathoexcitatory response in myocardial infarction rats via NF- κB and MAPK pathways.
P2X7 receptor regulates sympathoexcitatory response in myocardial infarction rats via NF-κB and MAPK pathways. Am J Transl Res. 2017;9(11):4954-4962 Authors: Wu Q, Xu H, Hao L, Ma G, Sun J, Song X, Ding F, Wang N Abstract Previous studies have provided evidence for the regulatory effect of P2X7 receptor (P2X7R) on cardiovascular activities. Our study focused on exploring the function and fundamental mechanism of microglial P2X7R in controlling sympathoexcitatory response using rats with acute myocardial infarction (AMI). Coronary artery ligation was used in rats to cause AMI. And before that, rats wer...
Source: American Journal of Translational Research - December 10, 2017 Category: Research Tags: Am J Transl Res Source Type: research

MicroRNA-1825 induces proliferation of adult cardiomyocytes and promotes cardiac regeneration post ischemic injury.
Authors: Pandey R, Velasquez S, Durrani S, Jiang M, Neiman M, Crocker JS, Benoit JB, Rubinstein J, Paul A, Ahmed RP Abstract In mammals, proliferative capacity of cardiomyocytes is lost soon after birth, while zebrafish and other lower organisms like newts are known to regenerate injured hearts even at an adult age. Here, we show that miR-1825 can induce robust proliferation of adult rat cardiomyocytes and can improve cardiac function in-vivo post myocardial infarction. Rat adult cardiomyocytes transfected with miR-1825 showed a significant increase in DNA synthesis, mitosis, cytokinesis, and an increase in cell nu...
Source: American Journal of Translational Research - July 5, 2017 Category: Research Tags: Am J Transl Res Source Type: research

Hypoxia-inducible factor 1 α protects mesenchymal stem cells against oxygen-glucose deprivation-induced injury via autophagy induction and PI3K/AKT/mTOR signaling pathway.
In conclusion, these data suggest that Hif-1α overexpression protects MSCs from OGD-induced injury via a mechanism in which autophagy and PI3K/AKT/mTOR pathway are implicated. PMID: 28559999 [PubMed]
Source: American Journal of Translational Research - June 2, 2017 Category: Research Tags: Am J Transl Res Source Type: research

Inhibition of MiR-92a May Protect Endothelial Cells After Acute Myocardial Infarction in Rats: Role of KLF2/4.
CONCLUSIONS MiR-92a was involved in the endothelial injury process after AMI and was able to suppress KLF2 and KLF4 expression. PMID: 27411964 [PubMed - in process]
Source: Medical Science Monitor - July 16, 2016 Category: Research Tags: Med Sci Monit Source Type: research

PEDF and PEDF-derived peptide 44mer stimulate cardiac triglyceride degradation via ATGL
Background: Pigment epithelium-derived factor (PEDF) is a 50-kDa secreted glycoprotein that is highly expressed in cardiomyocytes. A variety of peptides derived from PEDF exerts diverse physiological activities including anti-angiogenesis, antivasopermeability, and neurotrophic activities. Recent studies demonstrated that segmental functional peptides of PEDF, 44mer peptide (Val78–Thr121), show similar neurotrophic and cytoprotective effect to that of the holoprotein. We found that PEDF can reduce infarct size and protect cardiac function after acute myocardial infarction (AMI). However, the effects of PEDF on cardiac tr...
Source: Journal of Translational Medicine - February 21, 2015 Category: Research Authors: Hao ZhangTeng SunXia JiangHongli YuMeng WangTengteng WeiHuazhu CuiWei ZhuangZhiwei LiuZhongming ZhangHongyan Dong Source Type: research