Filtered By:
Condition: Heart Attack

This page shows you your search results in order of date. This is page number 14.

Order by Relevance | Date

Total 280 results found since Jan 2013.

S1P-S1PR2 Axis Mediates Homing of Muse Cells into Damaged Heart for Long Lasting Tissue Repair and Functional Recovery After Acute Myocardial Infarction.
Conclusions: Muse cells may provide reparative effects and robust functional recovery, and may thus provide a novel strategy for the treatment of AMI. PMID: 29475983 [PubMed - as supplied by publisher]
Source: Circulation Research - February 23, 2018 Category: Cardiology Authors: Yamada Y, Wakao S, Kushida Y, Minatoguchi S, Mikami A, Higashi K, Baba S, Shigemoto T, Kuroda Y, Kanamori H, Amin M, Kawasaki M, Nishigaki K, Taoka M, Isobe T, Muramatsu C, Dezawa M, Minatoguchi S Tags: Circ Res Source Type: research

MicroRNA-298 regulates apoptosis of cardiomyocytes after myocardial infarction.
CONCLUSIONS: MiR-298 can improve the myocardial apoptosis through the target gene BAX. PMID: 29424914 [PubMed - in process]
Source: European Review for Medical and Pharmacological Sciences - February 11, 2018 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

A positive feedback loop between IL-1 β, LPS and NEU1 may promote atherosclerosis by enhancing a pro-inflammatory state in monocytes and macrophages.
A positive feedback loop between IL-1β, LPS and NEU1 may promote atherosclerosis by enhancing a pro-inflammatory state in monocytes and macrophages. Vascul Pharmacol. 2018 Jan 22;: Authors: Sieve I, Ricke-Hoch M, Kasten M, Battmer K, Stapel B, Falk CS, Leisegang MS, Haverich A, Scherr M, Hilfiker-Kleiner D Abstract Inflammation plays an important role in atherosclerosis, a notion supported by the beneficial effects of the IL-1β inhibitor canakinumab in the CANTOS trial. Sialic acids (Sias), components of the surface glycocalyx, regulate intercellular and intermolecular interactions. We investigated ...
Source: Vascular Pharmacology - January 22, 2018 Category: Drugs & Pharmacology Authors: Sieve I, Ricke-Hoch M, Kasten M, Battmer K, Stapel B, Falk CS, Leisegang MS, Haverich A, Scherr M, Hilfiker-Kleiner D Tags: Vascul Pharmacol Source Type: research

MYBL2 protects against H9c2 injury induced by hypoxia via AKT and NF ‑κB pathways.
MYBL2 protects against H9c2 injury induced by hypoxia via AKT and NF‑κB pathways. Mol Med Rep. 2018 Jan 08;: Authors: Shao M, Ren Z, Zhang R Abstract Cardiovascular diseases have become one of the major public health problems in many countries. The downregulation of MYBL2 was found in H9c2 and native cardiomyocytes cells after hypoxia treatment. The present study aimed to investigate the effects of MYB proto‑oncogene like 2 (MYBL2) on H9c2 injury induced by hypoxia. Reverse transcription‑quantitative polymerase chain reaction and western blot were performed on H9c2 cells to determine the mRNA an...
Source: Molecular Medicine Reports - January 14, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Heparan sulfate potentiates leukocyte adhesion on cardiac fibroblast by enhancing Vcam-1 and Icam-1 expression
Conclusion These data show the dual role of HS during the initial stages of wound healing. Initially, HS enhance the pro-inflammatory role of CF increasing cytokines secretion; and later, by increasing protein adhesion molecules allows the adhesion of SMC on CF, which trigger CF-to-CMF differentiation.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - January 4, 2018 Category: Molecular Biology 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-210-mediated proliferation, survival, and angiogenesis promote cardiac repair post myocardial infarction in rodents
AbstractAn innovative approach for cardiac regeneration following injury is to induce endogenous cardiomyocyte (CM) cell cycle re-entry. In the present study, CMs from adult rat hearts were isolated and transfected with cel-miR-67 (control) and rno-miR-210. A significant increase in CM proliferation and mono-nucleation were observed in miR-210 group, in addition to a reduction in CM size, multi-nucleation, and cell death. When compared to control, β-catenin and Bcl-2 were upregulated while APC (adenomatous polyposis coli), p16, and caspase-3 were downregulated in miR-210 group. In silico analysis predicted cell cycle inhi...
Source: Journal of Molecular Medicine - September 25, 2017 Category: Molecular Biology Source Type: research

GSE94661 Smooth muscle cell-specific deletion of Col15a1 unexpectedly leads to impaired development of advanced atherosclerotic lesions
Contributors : Brittany G Durgin ; Olga A Cherepanova ; Delphine Gomez ; Themistoclis Karaoli ; Gabriel F Alencar ; Joshua T Butcher ; Yuging Zhou ; Michelle P Bendeck ; Brant E Isakson ; Gary K Owens ; Jessic J ConnelySeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAtherosclerotic plaque rupture with subsequent embolic events is a major cause of sudden death from myocardial infarction or stroke. Although smooth muscle cells (SMC) produce and respond to collagens in vitro, there is no direct evidence in vivo that SMC are a critical source of collagens impacting lesion development or f...
Source: GEO: Gene Expression Omnibus - September 8, 2017 Category: Genetics & Stem Cells Tags: Expression profiling by high throughput sequencing Mus musculus Source Type: research

Interaction of small G protein signaling modulator 3 with connexin 43 contributes to myocardial infarction in rat hearts.
Abstract Connexin 43 (Cx43), a ubiquitous connexin expressed in the heart and skin, is associated with a variety of hereditary conditions. Therefore, the characterization of Cx43-interacting proteins and their dynamics is important to understand not only the molecular mechanisms underlying pathological malfunction of gap junction-mediated intercellular communication but also to identify novel and unanticipated biological functions of Cx43. In the present study, we observed potential targets of Cx43 to determine new molecular functions in cardio-protection. MALDI-TOF mass spectrometry analysis of Cx43 co-immunoprec...
Source: Biochemical and Biophysical Research communications - August 31, 2017 Category: Biochemistry Authors: Lee CY, Choi JW, Shin S, Lee J, Seo HH, Lim S, Lee S, Joo HC, Kim SW, Hwang KC Tags: Biochem Biophys Res Commun Source Type: research

Danshensu accelerates angiogenesis after myocardial infarction in rats and promotes the functions of endothelial progenitor cells through SDF-1 α/CXCR4 axis.
Danshensu accelerates angiogenesis after myocardial infarction in rats and promotes the functions of endothelial progenitor cells through SDF-1α/CXCR4 axis. Eur J Pharmacol. 2017 Aug 29;: Authors: Yin Y, Duan J, Guo C, Wei G, Wang Y, Guan Y, Mu F, Yao M, Xi M, Wen A Abstract The present study was performed to investigate the the potential role of Danshensu in therapeutic angiogenesis in ischemic myocardium and endothelial progenitor cells (EPCs) function. The rat model of myocardial infarction (MI) injury was induced by left anterior descending coronary artery ligation for 14 days. Danshensu signific...
Source: European Journal of Pharmacology - August 29, 2017 Category: Drugs & Pharmacology Authors: Yin Y, Duan J, Guo C, Wei G, Wang Y, Guan Y, Mu F, Yao M, Xi M, Wen A Tags: Eur J Pharmacol 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

Small Interfering RNA Mediated Knockdown of Irisin Suppresses Food Intake and Modulates Appetite Regulatory Peptides in Zebrafish.
Abstract Irisin is a myokine encoded in fibronectin type III domain containing 5 (FNDC5). FNDC5 forms an integral part of the muscle post-exercise, and causes an increase in energy expenditure in mammals. Irisin is abundantly expressed in cardiac and skeletal muscles and is secreted upon activation of peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1 alpha). Irisin regulates feeding behaviour and cardiovascular function in mammals. More recently, irisin has gained importance as a potential biomarker for myocardial infarction due to its abundance in cardiac muscle. The goal of this research was ...
Source: General and Comparative Endocrinology - June 27, 2017 Category: Endocrinology Authors: Sundarrajan L, Unniappan S Tags: Gen Comp Endocrinol Source Type: research

Androgen inhibits key atherosclerotic processes by directly activating ADTRP transcription
In this study, we identified the molecular mechanism by which androgen regulates ADTRP expression and tested the hypothesis that androgen plays a protective role in cardiovascular disease by activating ADTRP expression. Luciferase assays with an ADTRP promoter luciferase reporter revealed that androgen regulated ADTRP transcription in a dose-and time-dependent manner, and the effect was abolished by three different androgen inhibitors, including pyrvinium pamoate, bicalutamide, and cyproterone acetate. Chromatin-immunoprecipitation showed that the androgen receptor bound to a half androgen response element (ARE, TGTTCT) lo...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - June 20, 2017 Category: Molecular Biology 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

Ghrelin suppresses inflammation in HUVECs by inhibiting ubiquitin-mediated uncoupling protein  2 degradation.
In this study, we demonstrate that the treatment of human umbilical vein endothelial cells (HUVECs) with ghrelin inhibits the oxidized low-density lipoprotein (oxLDL)-induced inflammatory response, In addition, treatment with ghrelin led to the accumulation of uncoupling protein 2 (UCP2) in the cells, thus decreasing reactive oxygen species (ROS) generation. Moreover, the siRNA-mediated knockdown of UCP2 expression suggested that the inhibitory effects of ghrelin on the inflammatory response relied on its ability to induce the accumulation of cellular UCP2 levels. Further analysis indicated that the accumulation of UC...
Source: International Journal of Molecular Medicine - May 13, 2017 Category: Molecular Biology Authors: Zhang R Tags: Int J Mol Med Source Type: research