Intracellular Zinc: A mediator of Vascular Aging and Disease?
Intracellular Zinc: A mediator of Vascular Aging and Disease?
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 manuscript which has been spread to the widest audience of experts; and thus increased in readership, citations and altimetry score.
Title: “Intracellular Zinc: A mediator of Vascular Aging and Disease?”
Abstract: Aging is a major risk factor in the development of cardiovascular diseases. Accumulation of waste materials like damaged mitochondria and decline in stress response mechanisms contribute to increased oxidative stress over time. The free radical theory of aging postulates that increased levels of reactive oxygen species [ROS] cause genomic and mitochondrial DNA damage leading to sustained oxidative stress that promotes tissue dysfunction and aging. In the cardiovascular system, NADPH oxidases produce ROS that are involved in normal function; however, overproduction of ROS by these enzymes, as well as decreased expression of antioxidant enzymes are associated with vascular dysfunction and disease.
Cellular senescence, a hallmark of mammalian aging, is a process of permanent cell cycle arrest that has been linked to the development of age-related diseases, including atherosclerosis. A causative role for senescence in disease development was reported as the selective removal of senescent cells in vivo showed a delay in age-related diseases. Although senescent cells have lost their replicative capability, they possess a secretory and pro-oxidative/inflammatory phenotype that likely contributes to organ dysfunction during aging.
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
Media Contact:
Steven Edwards
Editorial Assistant
Atherosclerosis: Open Access