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Condition: Heart Attack
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Total 280 results found since Jan 2013.
Delivery of Nox2-NADPH oxidase siRNA with polyketal nanoparticles for improving cardiac function following myocardial infarction.
This study highlights the potential of polyketals as siRNA delivery vehicles to the MI heart and represents a viable therapeutic approach for targeting oxidative stress.
PMID: 23856052 [PubMed - as supplied by publisher]
Source: Biomaterials - July 12, 2013 Category: Materials Science Authors: Somasuntharam I, Boopathy AV, Khan RS, Martinez MD, Brown ME, Murthy N, Davis ME Tags: Biomaterials Source Type: research
Nanocarriers Assisted siRNA Gene Therapy for the Management of Cardiovascular Disorders.
This article reviews the application of siRNA against CVDs with special emphasis on gene targets in combination with delivery systems such as cationic hydrogels, polyplexes, peptides, liposomes and dendrimers.
PMID: 26471319 [PubMed - in process]
Source: Current Pharmaceutical Design - October 18, 2015 Category: Drugs & Pharmacology Authors: Maheshwari R, Tekade M, Sharma PA, Tekade RK Tags: Curr Pharm Des Source Type: research
Ultrasound ‑targeted microbubble destruction‑mediated Galectin‑7‑siRNA promotes the homing of bone marrow mesenchymal stem cells to alleviate acute myocardial infarction in rats.
In conclusion, the present study demonstrated that UTMD‑mediated Galectin‑7‑siRNA treatment could enhance the homing ability of BMSCs, thus alleviating AMI in rats.
PMID: 33416139 [PubMed - as supplied by publisher]
Source: International Journal of Molecular Medicine - December 23, 2020 Category: Molecular Biology Authors: Wei X, Zheng Y, Zhang W, Tan J, Zheng H Tags: Int J Mol Med Source Type: research
Cardiac RNAi therapy using RAGE siRNA/deoxycholic acid-modified polyethylenimine complexes for myocardial infarction.
Abstract
Inflammatory response in myocardial ischemia-reperfusion injury plays a critical role in ventricular remodeling. To avoid deleterious effects of overwhelming inflammation, we blocked the expression of receptor for advanced glycation end-products (RAGE), a key mediator of the local and systemic inflammatory responses, via RNAi mechanism. Herein, a facial amphipathic deoxycholic acid-modified low molecular weight polyethylenimine (DA-PEI) was used as a siRNA delivery carrier to myocardium. The DA-PEI conjugate formed a stable complex with siRNA via electrostatic and hydrophobic interactions. The siRAGE/DA-P...
Source: Biomaterials - June 7, 2014 Category: Materials Science Authors: Hong J, Ku SH, Lee MS, Jeong JH, Mok H, Choi D, Kim SH Tags: Biomaterials Source Type: research
Deoxycholic acid-modified polyethylenimine based nanocarriers for RAGE siRNA therapy in acute myocardial infarction.
Abstract
The activation of receptor for advanced glycation end products (RAGE) signaling is mainly associated with myocardial ischemia/reperfusion injury. Thus the blockade of RAGE-ligands axis can be considered as a potential therapeutic strategy to protect myocardial infarction after ischemia/reperfusion injury. Herein, we strengthened the cardioprotective effect with combinatorial treatment of soluble RAGE (sRAGE) and RAGE siRNA (siRAGE) causing more effective suppression of RAGE-mediated signaling transduction. For pharmacological blockade of RAGE, sRAGE, the extracellular ligand binding domain of RAGE, acts a...
Source: Archives of Pharmacal Research - January 6, 2015 Category: Drugs & Pharmacology Authors: Ku SH, Hong J, Moon H, Jeong JH, Mok H, Park S, Choi D, Kim SH Tags: Arch Pharm Res 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
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
Protective effect of MAPK signaling pathway mediated by ITGB3 gene silencing on myocardial ischemia-reperfusion injury in mice and its mechanism.
CONCLUSIONS: Silencing ITGB3 gene expression can promote the activation of MAPK signaling pathway, elevate the phosphorylation of GSK-3β and Cx43 in the downstream, promote the proliferation of mouse myocardial cells, inhibit myocardial cell apoptosis and inflammatory reaction, and thus have protective effect on MIRI in mice.
PMID: 33577037 [PubMed - as supplied by publisher]
Source: European Review for Medical and Pharmacological Sciences - February 14, 2021 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research
Effect of miR-26a targeting GSK-3 β/β-catenin signaling pathway on myocardial apoptosis in rats with myocardial ischemia-reperfusion.
CONCLUSIONS: Knockdown of miR-26a could significantly improve I/R-induced myocardial injury and promote cardiac function in rats. The possible underlying mechanism might be related to targeted regulation of miR-26a on GSK-3β/β-catenin signaling pathway. Therefore, miR-26a was expected to be a new therapeutic target for myocardial I/R injury.
PMID: 31486509 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - September 7, 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
Reducing brain TACE activity improves neuroinflammation and cardiac function in heart failure rats
Tumor necrosis factor (TNF)-α converting enzyme (TACE) is a key metalloprotease mediating ectodomain shedding of a variety of inflammatory mediators, substrates, and growth factors. We previously reported that TACE-mediated production of TNF-α in the hypothalamic paraventricular nucleus (PVN) contributes to sympathetic excitation in heart failure (HF). Here, we sought to determine whether central interventions in TACE activity attenuate neuroinflammation and improve cardiac function in heart failure. Myocardial infarction-induced HF or sham-operated (SHAM) rats were treated with bilateral paraventricular nucleus microinj...
Source: Frontiers in Physiology - November 9, 2022 Category: Physiology Source Type: research
Mineralocorticoid and angiotensin II type 1 receptors in the paraventricular nucleus contribute to sympathetic hyperactivity and cardiac dysfunction in rats post myocardial infarction.
This article is protected by copyright. All rights reserved.
PMID: 24951624 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - June 20, 2014 Category: Physiology Authors: Huang BS, Chen A, Ahmad M, Wang HW, Leenen FH Tags: J Physiol Source Type: research
Specific inhibition of HDAC4 in cardiac progenitor cells enhances myocardial repairs
We have recently shown that in vivo inhibition of histone deacetylase (HDAC) stimulates endogenous myocardial regeneration in infarcted hearts (Zhang L et al. J Pharmacol Exp Ther 341: 285–293, 2012). Furthermore, our observation demonstrates that HDAC inhibition promotes cardiogenesis, which is associated with HDAC4 reduction. However, it remains unknown as to whether specific inhibition of HDAC4 modulates cardiac stem cells (CSCs) to facilitate myocardial repair and to preserve cardiac performance. c-kit+ CSCs were isolated from adult mouse hearts and were transfected with HDAC4 siRNA to knockdown HDAC4 of c-kit+ C...
Source: AJP: Cell Physiology - August 15, 2014 Category: Cytology Authors: Zhang, L. X., DeNicola, M., Qin, X., Du, J., Ma, J., Tina Zhao, Y., Zhuang, S., Liu, P. Y., Wei, L., Qin, G., Tang, Y., Zhao, T. C. Tags: ARTICLES Source Type: research
New cholesterol drug shows promise
Conclusion
Media headlines reporting on this phase I trial concentrated on the secondary outcome (that ALN-PCS reduced LDL cholesterol levels). However, these results will need to be confirmed during phase II and phase III clinical trials, which will involve more participants who would normally receive cholesterol-lowering treatment.
While it is tempting to focus on the results of the cholesterol levels, phase I clinical trials are designed to test the safety of a new drug to make sure it is safe enough to test further. They also aim to determine what the highest tolerable dose is, so the appropriate one can be used in la...
Source: NHS News Feed - October 3, 2013 Category: Consumer Health News Tags: Heart/lungs Medical practice Medication Source Type: news
Microglial P2X7 receptor in the hypothalamic paraventricular nuclei contributes to sympathoexcitatory responses in acute myocardial infarction rat
Publication date: 5 February 2015 Source:Neuroscience Letters, Volume 587 Author(s): Dongshu Du , Meiyan Jiang , Min Liu , Jin Wang , Chunmei Xia , Ruijuan Guan , Linlin Shen , Yonghua Ji , Danian Zhu Several pieces of evidence indicate that the microglial P2X7 receptor (P2X7R) regulate cardiovascular activities. We explored the possible roles of microglial P2X7R in the PVN mediated sympathoexcitatory responses in acute myocardial infarction (AMI) rat. Sprague–Dawley rats underwent coronary artery ligation to induce AMI. The rats received intraperitoneal administration of the P2X7R antagonist Brilliant Blue-G (BBG, 25 ...
Source: Neuroscience Letters - December 29, 2014 Category: Neuroscience Source Type: research
