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Condition: Heart Attack

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Total 280 results found since Jan 2013.

Cardiac Targeting Peptide : From Identification to Validation to Mechanism of Transduction.
Abstract Cell-penetrating peptides (CPPs), also known as protein transduction domains, were first identified 25 years ago. They are small, ~6-30 amino acid long, synthetic, or naturally occurring peptides, able to carry a variety of cargoes across the cellular membranes in an intact, functional form. These cargoes can range from other small peptides, full-length proteins, nucleic acids including RNA and DNA, nanoparticles, and viral particles as well as radioisotopes and other fluorescent probes for imaging purposes. However, this ability to enter all cell types indiscriminately, and even cross the blood-brain ba...
Source: Mol Biol Cell - December 19, 2020 Category: Molecular Biology Authors: Feldman KS, Pavlou MP, Zahid M Tags: Methods Mol Biol Source Type: research

Long Non-Coding RNA 554 Promotes Cardiac Fibrosis via TGF- β1 Pathway in Mice Following Myocardial Infarction
Conclusion: Collectively, our study illustrated the role of lncRNA 554 in cardiac fibrosis, suggested that lncRNA 554 might be a novel target for cardiac fibrosis.
Source: Frontiers in Pharmacology - December 16, 2020 Category: Drugs & Pharmacology Source Type: research

Down-regulation of Xist and Mir-7a-5p improves LPS-induced myocardial injury.
Conclusions: In this study, we established that down-regulation of xist and mir-7a-5p reduces apoptosis in response to LPS. PMID: 33029099 [PubMed - in process]
Source: International Journal of Medical Sciences - October 9, 2020 Category: Biomedical Science Tags: Int J Med Sci Source Type: research

MFGE8 is down-regulated in cardiac fibrosis and attenuates endothelial-mesenchymal transition through Smad2/3-Snail signalling pathway.
In conclusion, our experiments indicate that MFGE8 might play a protective role in TGF-β1-induced EndMT and might be a potential therapeutic target for cardiac fibrosis. PMID: 32945126 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - September 16, 2020 Category: Molecular Biology Authors: Wang B, Ge Z, Wu Y, Zha Y, Zhang X, Yan Y, Xie Y Tags: J Cell Mol Med Source Type: research

HIF-1 α-induced up-regulation of microRNA-126 contributes to the effectiveness of exercise training on myocardial angiogenesis in myocardial infarction rats.
In conclusion, we revealed that HIF-1α, whose expression experiences up-regulation during ET, could function as an upstream regulator to miR-126, resulting in angiogenesis promotion through the PI3K/AKT/eNOS and MAPK signalling pathway and subsequent improvement of the MI heart function. PMID: 32939968 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - September 15, 2020 Category: Molecular Biology Authors: Song W, Liang Q, Cai M, Tian Z Tags: J Cell Mol Med Source Type: research

Melatonin promotes cardiomyocyte proliferation and heart repair in mice with myocardial infarction via miR-143-3p/Yap/Ctnnd1 signaling pathway.
In this study, we investigated whether melatonin regulated cardiomyocyte proliferation and promoted cardiac repair in mice with myocardial infarction (MI), which was induced by ligation of the left anterior descending coronary artery. We showed that melatonin administration significantly improved the cardiac functions accompanied by markedly enhanced cardiomyocyte proliferation in MI mice. In neonatal mouse cardiomyocytes, treatment with melatonin (1 μM) greatly suppressed miR-143-3p levels. Silencing of miR-143-3p stimulated cardiomyocytes to re-enter the cell cycle. On the contrary, overexpression of miR-143-3p inhibi...
Source: Acta Pharmacologica Sinica - August 23, 2020 Category: Drugs & Pharmacology Authors: Ma WY, Song RJ, Xu BB, Xu Y, Wang XX, Sun HY, Li SN, Liu SZ, Yu MX, Yang F, Ye DY, Gong R, Han ZB, Yu Y, Bamba D, Wang N, Pan ZW, Cai BZ Tags: Acta Pharmacol Sin Source Type: research

Knockdown of endogenous RNF4 exacerbates ischaemia-induced cardiomyocyte apoptosis in mice.
Abstract RNF4, a poly-SUMO-specific E3 ubiquitin ligase, is associated with protein degradation, DNA damage repair and tumour progression. However, the effect of RNF4 in cardiomyocytes remains to be explored. Here, we identified the alteration of RNF4 from ischaemic hearts and oxidative stress-induced apoptotic cardiomyocytes. Upon myocardial infarction (MI) or H2 O2 /ATO treatment, RNF4 increased rapidly and then decreased gradually. PML SUMOylation and PML nuclear body (PML-NB) formation first enhanced and then degraded upon oxidative stress. Reactive oxygen species (ROS) inhibitor was able to attenuate the elev...
Source: J Cell Mol Med - July 27, 2020 Category: Molecular Biology Authors: Qiu F, Han Y, Shao X, Paulo P, Li W, Zhu M, Tang N, Guo S, Chen Y, Wu H, Zhao D, Liu Y, Chu W Tags: J Cell Mol Med Source Type: research

RP105 plays a cardioprotective role in myocardial ischemia reperfusion injury by regulating the Toll ‑like receptor 2/4 signaling pathways.
RP105 plays a cardioprotective role in myocardial ischemia reperfusion injury by regulating the Toll‑like receptor 2/4 signaling pathways. Mol Med Rep. 2020 Jun 16;: Authors: Huang W, Yang J, He C, Yang J Abstract The revascularization of blood vessels after myocardial infarction can lead to serious myocardial damage. Previous studies showed that radioprotective 105 kDa protein (RP105) is a specific negative regulator of myocardial ischemia reperfusion injury (MIRI). RP105 can modulate the Toll‑like receptor (TLR)2/TLR4 signaling pathways. However, the synergistic effect of TLR2/4 regulated by RP1...
Source: Molecular Medicine Reports - July 7, 2020 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Glutamyl-Prolyl-tRNA Synthetase Regulates Proline-Rich Pro-fibrotic Protein Synthesis During Cardiac Fibrosis.
Conclusions: Our results indicate that EPRS preferentially controls translational activation of proline codon rich pro-fibrotic genes in cardiac fibroblasts and augments pathological cardiac remodeling. PMID: 32611237 [PubMed - as supplied by publisher]
Source: Circulation Research - June 30, 2020 Category: Cardiology Authors: Wu J, Subbaiah KCV, Xie LH, Jiang F, Khor ES, Mickelsen DM, Myers JR, Tang WW, Yao P Tags: Circ Res Source Type: research

Diabetes mellitus exacerbates post ‐myocardial infarction heart failure by reducing sarcolipin promoter methylation
ConclusionsDiabetes increases the vulnerability of STEMI patients to post ‐MI HF by down‐regulating SLN promoter methylation, which further regulates SERCA2a activity via increasing cardiac SLN expression.
Source: ESC Heart Failure - June 10, 2020 Category: Cardiology Authors: Zhongwei Liu, Yong Zhang, Chuan Qiu, Haitao Zhu, Shuo Pan, Hao Jia, Hongyan Kang, Gongchang Guan, Rutai Hui, Ling Zhu, Junkui Wang Tags: Original Research Article Source Type: research

MiR-379 relieves myocardial injury after acute myocardial infarction by regulating tumor necrosis factor- α-induced protein 8.
CONCLUSIONS: MiR-379 has a binding site with TNFAIP8 and can inhibit its activity by binding to TNFAIP8 mRNA. SiRNA-TNFAIP8 can inhibit the NF-κB signaling pathway and protect myocardial cells from AMI-induced myocardial damage by reducing the apoptosis level of myocardial cells. PMID: 32414226 [PubMed - as supplied by publisher]
Source: Panminerva Medica - May 17, 2020 Category: General Medicine Tags: Panminerva Med Source Type: research

Inhibition of TGF β-activated protein kinase 1 ameliorates myocardial ischaemia/reperfusion injury via endoplasmic reticulum stress suppression.
Inhibition of TGFβ-activated protein kinase 1 ameliorates myocardial ischaemia/reperfusion injury via endoplasmic reticulum stress suppression. J Cell Mol Med. 2020 May 07;: Authors: Zeng J, Jin Q, Ruan Y, Sun C, Xu G, Chu M, Ji K, Wu L, Li L Abstract Transforming growth factor β-activated protein kinase 1 (TAK1) involves in various biological responses and is a key regulator of cell death. However, the role of TAK1 on acute myocardial ischaemia/reperfusion (MI/R) injury is unknown. We observed that TAK1 activation increased significantly after MI/R and hypoxia/reoxygenation (H/R), and we hypothesiz...
Source: J Cell Mol Med - May 6, 2020 Category: Molecular Biology Authors: Zeng J, Jin Q, Ruan Y, Sun C, Xu G, Chu M, Ji K, Wu L, Li L Tags: J Cell Mol Med Source Type: research

Downregulation of miRNA-663b protects against hypoxia-induced injury in cardiomyocytes by targeting BCL2L1.
In conclusion, miR-663b inhibition protected cardiomyocytes against hypoxia-induced injury by targeting BCL2L1 and may potentially be a novel target for the treatment of patients with myocardial infarction. PMID: 32346421 [PubMed]
Source: Experimental and Therapeutic Medicine - April 30, 2020 Category: General Medicine Tags: Exp Ther Med 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

Danqi Pill Protects Against Heart Failure Post-Acute Myocardial Infarction via HIF-1 α/PGC-1α Mediated Glucose Metabolism Pathway
ConclusionsDQP exhibits the efficacy to improve myocardial glucose metabolism, mitochondrial oxidative phosphorylation and biogenesis by regulating HIF-1α/PGC-1α signaling pathway in HF post-AMI rats.
Source: Frontiers in Pharmacology - April 20, 2020 Category: Drugs & Pharmacology Source Type: research