Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35

The aim of the work was to examine the degree of carotid stenosis, the structure of atherosclerotic plaques, and the predominance of the main vascular risk factors in patients with multiple lacunar and comparatively large "non-lacunar" cerebral infarctions. A study WAS made of the data on 110 patients (mean age 62.5 years) with multiple cerebral infarctions revealed by MRT and with stenoses of the internal carotid artery (ICA) of varying degrees of severity. Minor lacunar infarctions (LI) were present in 62 cases whereas comparatively large "non-lacunar" infarctions (NLI) in 48 cases. All the patients underwent standard neurologic examination, laboratory analyses, MRT of the brain with angiography (MRA) of the extra-intrecrania1 vessels, transcranial Doppler (TCD), and examination of the heart for revealing the cardioembolic nature of cerebral infarctions. Among patients with both LI and NLI, arterial hypertension was the most frequently occurring risk factor in 53 (85%) and 35 (73%) patients respectively. In the study groups, there were no appreciable differences in the incidence of high hematocrit, hyperfibrinogenemia, tobacco-smoking, and diabetes mellitus. Patients with NLI demonstrated hypercholesterolemia, CAD and atherosclerosis of the peripheral vessels significantly more often (p<0.05). In the patient group with NLI, hemodynamically significant stenoses of the ICA were predominant: in 18 (37.5%) patients, they were moderate, in 12 (25%) critical, and 7 (14.6%) patients had occlusions whereas in LI, the portion of critical stenoses and ICA occlusions was cooperatively low - in 11 (17.7%) and in 5 (8.1%) patients respectively. Both groups showed the thickening of the complex of the medial CCA layer. Ultrasonopraphy of the vessels has revealed that in patients with NLI and LI, there predominated potentially embologenic plaques, namely in 69% and in 53% of cases, respectively. Our investigations allow to assume that arterial hypertension is the most frequently occurring risk factor of cerebral infarction (both minor lacunar and large "non-lacunar"). Factors such as CAD, hypercholesterolemia, DM, hemorheological disorders, end tobacco-smoking are likely to have an unfavorable impact on both general and cerebral hemodynamics as well as on the microcirculatory bed whereby being on the whole important risk factors of cerebral infarction. Hemodynamically significant stenoses, especially critical ones, occlusions, and embologenic plaques of the ICA are pathogenetically closely linked with the development of "non-lacunar" cerebral infarctions. At the same time they, under certain conditions, may become the cause of multiple lacunar cerebral infarctions.
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PMID:[The status of carotid arteries and the main vascular risk factors in cerebral infarctions of "anterior circulation"]. 1516 92

Familial hypercholesterolemia (FH) is a genetic disorder characterized by a high serum concentration of low-density lipoprotein (LDL) cholesterol. The high LDL cholesterol level leads to an excess deposition of cholesterol in the arterial walls and accelerated atherosclerosis, thereby increasing the risk of premature coronary heart disease. In the present study, we used a DNA microarray approach to identify gene expression profiles that distinguish patients with FH from healthy control subjects. Furthermore, transcription factors (TFs), microRNAs (miRNAs), target genes and pathways were analyzed to explore the potential transcriptional interactions occurring in FH. Publicly available microarray and regulation data were used to construct a regulatory network to identify additional genes related to FH and their interactions. The results revealed that specificity protein 1 (SP1), signal transducer and activator of transcription 1 (STAT1) and spleen focus forming virus (SFFV) proviral integration oncogene spi1 (SPI1) play a central role in the FH regulatory network. In addition, the TF, upstream transcription factor 2, c-fos interacting (USF2) and the gene, Wiskott-Aldrich syndrome (WAS), were identified to be associated with FH, although no reports for these proteins exist in the literature. Overall, transcriptional network analysis proved to be effective approach to identify novel targets for FH therapy.
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PMID:Transcriptome and miRNA network analysis of familial hypercholesterolemia. 2437 67

To investigate the role of small nucleolus RNA host gene 14 (SNHG14) in the progression of atherosclerosis (AS), bioinformatics analysis, and other relevant experiments (cell counting kit-8, flow cytometry, quantitative real-time polymerase chain reaction, luciferase reporter, RNA immunoprecipitation, RNA pull-down, and western blot assays) were done. The current study revealed that SNHG14 level was high in the serum of AS patients and oxidized low-density lipoprotein (ox-LDL)-induced AS cell lines. Besides, we found that SNHG14 accelerated cell proliferation while inhibited cell apoptosis in ox-LDL-induced AS cell lines. Next, SNHG14 was confirmed to be a sponge for miR-186-5p in AS cells, and it was validated that SNHG14 regulated AS cell proliferation and apoptosis by sponging miR-186-5p. Moreover, we uncovered that WAS-interacting protein family member 2 (WIPF2) was a downstream target of miR-186-5p in AS cells. Finally, it was demonstrated that miR-186-5p modulated AS cell proliferation and apoptosis via targeting WIPF2. To conclude, our research disclosed that SNHG14 affected ox-LDL-induced AS cell proliferation and apoptosis through miR-186-5p/WIPF2 axis, which may provide a theoretical basis for the treatment and diagnosis of AS.
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PMID:Long noncoding RNA SNHG14 regulates ox-LDL-induced atherosclerosis cell proliferation and apoptosis by targeting miR-186-5p/WIPF2 axis. 3273 35