Investigating the Effect of Phenylbutyrate and Valproate Supplementation on Atherosclerotic Plaque Regression in a High Fat Diet Fed LDLR-/- Mouse Model
Investigating the Effect of Phenylbutyrate and Valproate Supplementation on Atherosclerotic Plaque Regression in a High Fat Diet Fed LDLR-/- Mouse Model
Atherosclerosis: Open Access (Omics Publishing S.L) has announced almost 50 % discount on article processing charge to commemorate its 10th Anniversary.
Atherosclerosis: Open Access is an open access, peer-reviewed journal that focuses and welcomes submissions on all aspects of Coronary Heart disease, Stroke, Peripheral Arterial Disease, Chronic Kidney Disease, arteriosclerosis, Coronary Atherosclerosis, intracranial atherosclerosis etc.
It gives us great pleasure to announce the call for paper on the occasion of 10th Anniversary of the Journal at special and hefty discount of up to 50 % on one-time article processing charge. Prospective academicians and scientists are encouraged to utilize this opportunity to get their articles reviewed, processed and published at relatively faster pace and at lower charges. In addition to this, the authors who publish with us during the year-long celebrations will also be eligible for academic awards recommended by the editorial panel.
The Archive page contains wide variety of articles such as Research / Review / Case reports / short communication / Mini review / Prospective / Letter to Editors Etc. We would like introduce a Research article which has been spread to the widest audience of experts; and thus increased in readership, citations and altimetry score.
Abstract: Evidence suggests that Endoplasmic Reticulum (ER) stress plays a causative role in the development of atherosclerosis. Our previous studies have shown that ER stress signals through glycogen synthase kinase (GSK)-3αβ to activate pro-atherogenic pathways. The purpose of this study is to determine if small molecule inhibitors of ER stress-GSK3αβ signaling can promote the regression of existing atherosclerotic lesions. Four-week-old female low density lipoprotein receptor deficient (LDLR-/-) mice were fed a high fat diet for 16 weeks to establish atherosclerotic lesions. A subset of mice was sacrificed at this time to set the baseline for atherosclerotic progression. The remaining mice were switched to stand chow diet (control) or a standard chow diet supplemented with phenyl butyrate, a chemical chaperone that reduces ER stress, or valproate, a branch chain fatty acid that selectively inhibits GSK3αβ. These mice were harvested at 30 weeks of age and atherosclerotic lesions were quantified and characterized. Dietary supplementation with phenyl butyrate and valproate had no effect on body weight but did significantly reduce plasma cholesterol levels. Atherosclerotic lesion areas at the aortic sinus and total atherosclerotic volumes were significantly larger in the control group compared to the baseline group, indicating that the lesions continued to grow despite the switch from a high fat diet to chow diet. The supplemented mice had significantly smaller lesions than the control group, but not the baseline group. Both phenyl butyrate and valproate supplementation reduced lesional macrophage/foam cell content and necrotic core area, and increased smooth muscle cell content and collagen content, relative to control and baseline groups. These changes are indicative of more stable atherosclerotic lesions. Small molecule inhibitors of ER stress-GSK3αβ signaling do attenuate the growth of existing atherosclerotic lesions and appear to increase lesion stability. It remains unclear whether these interventions can actually promote atherosclerotic regression.
To have a glance at the full length manuscript, you can visit us at our archive page and Currently, Journal’s Archive is holding not only normal issues but also focusing on special issues. The purpose of special issues is to publish the most exciting research with respect to the subjects of Atherosclerosis / Cardiovascular Diseases and to provide a rapid turn-around time regarding reviewing and publishing, and to publicize the articles freely for research, teaching and reference purposes. Submit manuscript of your research articles or special issue articles online through manuscript submission or forwarded to the Editorial Office at atherosclerosis@oajournal.org
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