VASCULAR PHARMACOLOGY
血管药理学
ISSN: 1537-1891
自引率: 1.9%
发文量: 78
被引量: 3141
影响因子: 5.732
通过率: 暂无数据
出版周期: 月刊
审稿周期: 7
审稿费用: 0
版面费用: 暂无数据
年文章数: 78
国人发稿量: 9

投稿须知/期刊简介:

Published by Elsevier Science. ISSN: 1537-1891.<br /><br />Vascular Pharmacology publishes papers, written in English, which contain results of all aspects of pharmacology of the vascular system. Papers are encouraged in all areas, including angiogenesis, growth factors, nitric oxide, cell signaling, vasoactive mediators, hypertension, atherosclerosis, metabolic diseases, blood element-vessel wall interactions, thrombosis, microcirculation, vascular developmental biology and remodeling, vascular inflammation and immunity. Papers are encouraged on pharmacological research utilizing approaches ranging from molecular biology to integrative physiology.

期刊描述简介:

Vascular Pharmacology publishes papers, which contains results of all aspects of biology and pharmacology of the vascular system. Papers are encouraged in basic, translational and clinical aspects of Vascular Biology and Pharmacology, utilizing approaches ranging from molecular biology to integrative physiology. All papers are in English. The Journal publishes review articles which include vascular aspects of thrombosis, inflammation, cell signalling, atherosclerosis, and lipid metabolism. Benefits to authors We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services . Please see our Guide for Authors for information on article submission. If you require any further information or help, please visit our Support Center.

最新论文
  • Altered copper transport in oxidative stress-dependent brain endothelial barrier dysfunction associated with Alzheimer's disease.

    被引量:- 发表:1970

  • Matrix metalloproteinases in aortic dissection.

    Aortic dissection, characterized by a high immediate mortality, is primarily caused by excessive bleeding within the walls of the aorta or a severe tear within the intimal layer of the aorta. Inflammation, as well as oxidative stress and the degradation of extracellular matrix (ECM), are significant factors in the development and occurrence of aortic dissection. Matrix metalloproteinases (MMPs) are pivotal enzymes responsible for degrading the ECM. Inflammatory factors and oxidants can interact with MMPs, indicating the potential significance of MMPs in aortic dissection. A substantial body of evidence indicates that numerous MMPs are significantly upregulated in aortic dissection, playing a critical role in ECM degradation and the pathogenesis of aortic dissection. Furthermore, targeting these enzymes has demonstrated potential in facilitating ECM restoration and reducing the incidence of aortic dissection. This review initially provides a brief overview of MMP biology before delving into their expression patterns, regulatory mechanisms, and therapeutic applications in aortic dissection. A profound comprehension of the catabolic pathways associated with aortic dissection is imperative for the future development of potential preventive or therapeutic bio-interventions for aortic dissection.

    被引量:- 发表:1970

  • Macrophages in vascular disease: Roles of mitochondria and metabolic mechanisms.

    Macrophages are a dynamic cell type of the immune system implicated in the pathophysiology of vascular diseases and are a major contributor to pathological inflammation. Excessive macrophage accumulation, activation, and polarization is observed in aortic aneurysm (AA), atherosclerosis, and pulmonary arterial hypertension. In general, macrophages become activated and polarized to a pro-inflammatory phenotype, which dramatically changes cell behavior to become pro-inflammatory and infiltrative. These cell types become cumbersome and fail to be cleared by normal mechanisms such as autophagy. The result is a hyper-inflammatory environment causing the recruitment of adjacent cells and circulating immune cells to further augment the inflammatory response. In AA, this leads to excessive ECM degradation and chemokine secretion, ultimately causing macrophages to dominate the immune cell landscape in the aortic wall. In atherosclerosis, monocytes are recruited to the vascular wall, where they polarize to the pro-inflammatory phenotype and induce inflammatory pathway activation. This leads to the development of foam cells, which significantly contribute to neointima and necrotic core formation in atherosclerotic plaques. Pro-inflammatory macrophages, which affect other vascular diseases, present with fragmented mitochondria and corresponding metabolic dysfunction. Targeting macrophage mitochondrial dynamics has proved to be an exciting potential therapeutic approach to combat vascular disease. This review will summarize mitochondrial and metabolic mechanisms of macrophage activation, polarization, and accumulation in vascular diseases.

    被引量:- 发表:1970

  • Development of a dietary supplement with antioxidant and cardioprotective action. Phase 1: Absorption and biodistribution study.

    被引量:- 发表:2024

  • Prevention of cardiovascular complications in elderly cancer patients.

    被引量:- 发表:2024

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