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Editor Note: Atherosclerosis-Open Access
Atherosclerosis: Open Access

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  • Editorial   
  • Atheroscler Open Access 2016, Vol 1(2): e106

Editor Note: Atherosclerosis-Open Access

Tamer MA Mohamed*
Postdoctoral Research Associate, The University of Manchester, UK
*Corresponding Author: Tamer MA Mohamed, Postdoctoral Research Associate, The University of Manchester, UK, Email: Tamer.Mohamed@Manchester.ac.uk

Received: 24-Dec-2016 / Accepted Date: 25-Dec-2016 / Published Date: 30-Dec-2016

Editor Note

Atherosclerosis is a medical condition in which hardening and narrowing of the arteries occurs which slowly blocks the arteries and thus blood flow. The disease can be lethal as it may lead to heart attacks, strokes and other cardiovascular complications. Atherosclerosis: Open Access, journal aims to bring studies and researches related to a very interesting medical complication to the readers. The journal has successfully released its first issue with editorials, mini-reviews, and short communications related to the current advancement in the field of atherosclerosis research.

Liu in its mini-review explained that the post myocardial infarction inflammatory response is a part of cardiac repair pathways and also unfortunately is involved in the subsequent heart failure pathology [1]. In his research, Liu reported that FoxO4 promotes early inflammatory response by suppressing endothelial barrier. The researchers were also successful in providing a connection between FoxO4 and Arginase 1 and postulated that inhibition of arginase activity in myocardial infarction can reduce post-myocardial infarction inflammation. They suggested that FoxO4 may be a potential therapeutic target for post myocardial infarction heart repair and regeneration [1].

Mohamed in his short communication discussed the novel cell replacement strategies for Heart Failure treatment [2]. He detailed that cell replacement therapy has emerged as a novel approach in the treatment of heart failure. The theory behind this approach is that after myocardial infarction or in heart failure, lost cardiomyocytes can be replaced by adding either new cardiomyocytes or a potential source of cardiomyocytes such as stem cells. His literature review suggested that researchers have exploited skeletal myoblasts, cardiac progenitor cells and mesenchymal stem cells from bone marrow in this regard. However, the result achieved was not so enthusiastic. The reason behind this was that the stem cells do not Trans-differentiate into cardiomyocytes in-vivo and the number of stem cells retained in the heart after delivery is very low. In another attempt of cell-replacement therapy for heart failure using pluripotent stem cell derived cardiomyocytes showed better result in rodents and non-human primates [2].

Yamanaka et al., detailed the radiation induced arterial injury in the upper limb [3]. In his mini review discussed that radiation combination therapy for malignant tumors has improved cancer survival rate, thus increasing the importance of radiation therapy. However there have been many reports by the researchers about stenosis and obstruction of the blood vessels within the irradiated area following radiation therapy. Yamanaka and researchers are among the few researchers to report about the radiation induced arterial injury in the arteries of the upper limbs. The researchers suggested that irradiation can cause arteriosclerosis and a careful examination should be conducted in a larger sample size to better understand this medical complication [3].

References

  1. Liu ZP (2016) The Role of FoxO4 in Post-Myocardial Infarction Left Ventricular Remodeling. Atheroscler open access 1: 101.
  2. Mohamed TMA (2016) Novel Cell Replacement Strategies for Heart Failure Treatment. Atheroscler open access 1: 102.
  3. Tetsuo Y, Toru F, Yoshimaro I, Hirotaka K, Yasunobu H, et al. (2016) Radiation-Induced Arterial Injury in the Upper Limb . Atheroscler Open Access 1:103.

Citation: Mohamed T (2016) Editor Note: Atherosclerosis-Open Access. Atheroscler open access 1: e106.

Copyright: © 2016 Mohamed TMA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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