Example of Current Hypertension Reviews format
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Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format
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Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format Example of Current Hypertension Reviews format
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open access Open Access ISSN: 15734021 e-ISSN: 18756506

Current Hypertension Reviews — Template for authors

Publisher: Bentham Science
Categories Rank Trend in last 3 yrs
Internal Medicine #60 of 121 down down by None rank
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 82 Published Papers | 253 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 24/06/2020
Insights & related journals
General info
Top papers
Popular templates
Get started guide
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FAQ

Journal Performance & Insights

  • CiteRatio
  • SJR
  • SNIP

CiteRatio is a measure of average citations received per peer-reviewed paper published in the journal.

3.1

15% from 2019

CiteRatio for Current Hypertension Reviews from 2016 - 2020
Year Value
2020 3.1
2019 2.7
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 15% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR) measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

0.486

1% from 2019

SJR for Current Hypertension Reviews from 2019 - 2020
Year Value
2020 0.486
2019 0.49
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 1% in last years.
  • This journal’s SJR is in the top 10 percentile category.

Source Normalized Impact per Paper (SNIP) measures actual citations received relative to citations expected for the journal's category.

0.606

12% from 2019

SNIP for Current Hypertension Reviews from 2019 - 2020
Year Value
2020 0.606
2019 0.689
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has decreased by 12% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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CiteRatio: 5.9 | SJR: 1.039 | SNIP: 1.036
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CiteRatio: 6.0 | SJR: 1.141 | SNIP: 1.158
open access Open Access ISSN: 15226417 e-ISSN: 15343111

Springer

CiteRatio: 7.0 | SJR: 1.434 | SNIP: 1.502
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CiteRatio: 14.7 | SJR: 3.464 | SNIP: 2.542

Current Hypertension Reviews

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Bentham Science

Current Hypertension Reviews

Approved by publishing and review experts on SciSpace, this template is built as per for Current Hypertension Reviews formatting guidelines as mentioned in Bentham Science author instructions. The current version was created on 24 Jun 2020 and has been used by 126 authors to write and format their manuscripts to this journal.

i
Last updated on
24 Jun 2020
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ISSN
1573-4021
i
Impact Factor
Low - 0.129
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Open Access
No
i
Sherpa RoMEO Archiving Policy
Yellow faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
Vancouver
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder, G E, Tinkham, M, & Klapwijk, T M. Transition from metallic to tunnel- ing regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B. 2013;87(10):100510.

Top papers written in this journal

Journal Article DOI: 10.2174/1573402111666150529130922
Oxidative stress and antioxidants in hypertension-a current review.
Nakshi Sinha, Pradeep Kumar Dabla1

Abstract:

Free radicals or reactive oxygen species (ROS) are generated by oxygen metabolism which is balanced by the rate of oxidant formation and the rate of oxidant elimination. Oxidative stress is a result of imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defence systems. Hypertension is one of... Free radicals or reactive oxygen species (ROS) are generated by oxygen metabolism which is balanced by the rate of oxidant formation and the rate of oxidant elimination. Oxidative stress is a result of imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defence systems. Hypertension is one of the major risk factors for cardiovascular diseases and is considered as a leading cause of mortality and morbidity. These diseases affect more than 600 million people and it has been estimated that 29% of the world population will be suffering from hypertension by 2025. It has been indicated by experimental evidence that reactive oxygen species (ROS) play an important role in the pathophysiology of hypertension. The vasculature is a rich source of NADPH oxidase which produces most of the reactive oxygen species and plays an important role in renal dysfunction and vascular damage. Recent studies indicate that increased oxidative stress is the important mediator of endothelial injury in the pathology of hypertension associated to increased production of pro oxidants such as superoxideanion hydrogen peroxide, reduced nitric oxide synthesis and decreased bioavailability of antioxidants. Oxidative stress is found to be associated with endothelial dysfunction, inflammation, hypertrophy, apoptosis, cell migration, fibrosis, and angiogenesis in relation to vascular remodelling of hypertension. Results in humans are still less conclusive inspite of data available that involve oxidative stress as a causative factor of essential hypertension. The aim of this review is to present a novel focus on the role of oxidative stress in the pathophysiology of hypertension and recent biomarkers which are found to be associated with reactive oxygen species and the role of antioxidants as therapy of hypertension. read more read less

Topics:

Oxidative stress (62%)62% related to the paper, Free-radical theory of aging (62%)62% related to the paper, Pathophysiology of hypertension (60%)60% related to the paper, Endothelial dysfunction (56%)56% related to the paper, Essential hypertension (56%)56% related to the paper
174 Citations
open accessOpen access Journal Article DOI: 10.2174/157340208786241336
Role of Reactive Oxygen Species in Tumor Necrosis Factor-alpha Induced Endothelial Dysfunction.
Xiuping Chen1, Bradley T. Andresen, Michael A. Hill, Jing Zhang1, Frank W. Booth, Cuihua Zhang

Abstract:

Endothelial cell injury and dysfunction are the major triggers of pathophysiological processes leading to cardiovascular disease. Endothelial dysfunction (ED) has been implicated in atherosclerosis, hypertension, coronary artery disease, vascular complications of diabetes, chronic renal failure, insulin resistance and hyperch... Endothelial cell injury and dysfunction are the major triggers of pathophysiological processes leading to cardiovascular disease. Endothelial dysfunction (ED) has been implicated in atherosclerosis, hypertension, coronary artery disease, vascular complications of diabetes, chronic renal failure, insulin resistance and hypercholesterolemia. Although now recognized as a class of physiological second messengers, reactive oxygen species (ROS) are important mediators in cellular injury, specifically, as a factor in endothelial cell damage. Uncontrolled ROS production and/or decreased antioxidant activity results in a deleterious state referred to as 'oxidative stress'. A candidate factor in causing ROS production in endothelial cells is tumor necrosis factor alpha (TNF-α), a pleiotropic inflammatory cytokine. TNF-α has been shown to both be secreted by endothelial cells and to induce intracellular ROS formation. These observations provide a potential mechanism by which TNF-α may activate and injure endothelial cells resulting in ED. In this review, we focus on the relationship between intracellular ROS formation and ED in endothelial cells or blood vessels exposed to TNF-α to provide insight into the role of this important cytokine in cardiovascular disease. read more read less

Topics:

Endothelial dysfunction (63%)63% related to the paper, Endothelial stem cell (58%)58% related to the paper, Tumor necrosis factor alpha (55%)55% related to the paper, Cytokine (54%)54% related to the paper, Oxidative stress (54%)54% related to the paper
112 Citations
Journal Article DOI: 10.2174/157340211001141111160957
Brachial-ankle pulse wave velocity in the measurement of arterial stiffness: recent evidence and clinical applications.

Abstract:

Arterial stiffness is a vascular measure that has been reported to predict cardiovascular events. It is important to measure arterial stiffness in order to determine current vascular status and treatment strategy. Brachial-ankle pulse wave velocity (baPWV) is a unique measure of systemic arterial stiffness that is measured by... Arterial stiffness is a vascular measure that has been reported to predict cardiovascular events. It is important to measure arterial stiffness in order to determine current vascular status and treatment strategy. Brachial-ankle pulse wave velocity (baPWV) is a unique measure of systemic arterial stiffness that is measured by brachial and tibial arterial wave analyses. Measurement of baPWV is easy and is reproducible. For more than a decade, this measure has been used broadly in East Asian countries. Meta-analysis of cohort studies conducted in the general population with hypertension, diabetes, or end-stage renal disease, and other high-risk individuals have shown that a 1 m/s increase in baPWV is associated with 12% increase in the risk of cardiovascular events. Thus, the Japanese Circulation Society has proposed that a baPWV of 1800 cm/s is a threshold for high-risk category. For baPWV to be clinically applicable, we must confirm that circulation of the lower limbs are normal by examining brachial ankle blood pressure index. In cases of peripheral arterial disease, the reliability of baPWV measurement is attenuated. To further confirm the clinical usefulness of this measure, we need to examine the hypothesis that baPWV-guided therapy could improve prognosis in high-risk patients. read more read less

Topics:

Pulse wave velocity (66%)66% related to the paper, Arterial stiffness (58%)58% related to the paper, Blood pressure (53%)53% related to the paper, Population (51%)51% related to the paper
95 Citations
open accessOpen access Journal Article DOI: 10.2174/157340209788166940
Hyperhomocysteinemia and Endothelial Dysfunction.
Zhongjian Cheng1, Xiaofeng Yang, Hong Wang

Abstract:

Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in human and in animal models of HHcy induced by either high-methionine load or ge... Hyperhomocysteinemia (HHcy) is a significant and independent risk factor for cardiovascular diseases. Endothelial dysfunction (ED) is the earliest indicator of atherosclerosis and vascular diseases. We and others have shown that HHcy induced ED in human and in animal models of HHcy induced by either high-methionine load or genetic deficiency. Six mechanisms have been suggested explaining HHcy-induced ED. These include 1) nitric oxide inhibition, 2) prostanoids regulation, 3) endothelium-derived hyperpolarizing factors suppression, 4) angiotensin II receptor-1 activation, 5) endothelin-1 induction, and 6) oxidative stress. The goal of this review is to elaborate these mechanisms and to discuss biological and molecular events related to HHcy-induced ED. read more read less

Topics:

Angiotensin II (58%)58% related to the paper, Endothelial dysfunction (55%)55% related to the paper, Hyperhomocysteinemia (52%)52% related to the paper
94 Citations
open accessOpen access Journal Article DOI: 10.2174/157340210791170994
Leptin-Induced Sympathetic Nerve Activation: Signaling Mechanisms and Cardiovascular Consequences in Obesity.
Kamal Rahmouni1

Abstract:

Obesity increases cardiovascular morbidity and mortality in part by inducing hypertension. One factor linking excess fat mass to cardiovascular diseases may be the sympathetic cardiovascular actions of leptin. Initial studies of leptin showed it regulates appetite and enhances energy expenditure by activating sympathetic nerv... Obesity increases cardiovascular morbidity and mortality in part by inducing hypertension. One factor linking excess fat mass to cardiovascular diseases may be the sympathetic cardiovascular actions of leptin. Initial studies of leptin showed it regulates appetite and enhances energy expenditure by activating sympathetic nerve activity (SNA) to thermogenic brown adipose tissue. Further study, however, demonstrated leptin also causes sympathetic excitation to the kidney that, in turn, increases arterial pressure. In animal studies, elevating circulating leptin levels increased arterial pressure. Moreover, mice with diet-induced obesity have a preserved arterial pressure response to leptin despite the resistance to the metabolic action of leptin and these mice have elevated baseline arterial pressure. Conversely, severely obese, but leptin-deficient, mice and humans display low sympathetic tone and decreased blood pressure. Together, these findings demonstrate that leptin plays a physiological role in maintaining sympathetic tone and blood pressure, and further suggest that hyperleptinemia may contribute to the elevated blood pressure associated with obesity. Consistent with this selectivity in leptin resistance, mounting evidence suggests that the sympathetic nervous system subserving different tissues is differentially controlled by leptin. For instance, different molecular signaling mechanisms are engaged by the leptin receptor to control the regional sympathetic nerve activity. Understanding the mechanisms by which leptin controls the sympathetic nervous system will provide insight into the cardiovascular complications of obesity. read more read less

Topics:

Leptin receptor (72%)72% related to the paper, Leptin (61%)61% related to the paper, Sympathetic nervous system (55%)55% related to the paper, Appetite (53%)53% related to the paper, Blood pressure (53%)53% related to the paper
69 Citations
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Current Hypertension Reviews format uses Vancouver citation style.

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Frequently asked questions

Absolutely not! With our tool, you can freely write without having to focus on LaTeX. You can write your entire paper as per the Current Hypertension Reviews guidelines and autoformat it.

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Sure. We support all the top citation styles like APA style, MLA style, Vancouver style, Harvard style, Chicago style, etc. For example, in case of this journal, when you write your paper and hit autoformat, it will automatically update your article as per the Current Hypertension Reviews citation style.

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One little Google search can get you the Word template for any journal. However, why do you need a Word template when you can write your entire manuscript on SciSpace, autoformat it as per Current Hypertension Reviews's guidelines and download the same in Word, PDF and LaTeX formats? Try us out!.

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To be honest, the answer is NO. The impact factor is one of the many elements that determine the quality of a journal. Few of those factors the review board, rejection rates, frequency of inclusion in indexes, Eigenfactor, etc. You must assess all the factors and then take the final call.

SHERPA/RoMEO Database

We have extracted this data from Sherpa Romeo to help our researchers understand the access level of this journal. The following table indicates the level of access a journal has as per Sherpa Romeo Archiving Policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

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S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
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After signing up, you would need to import your existing references from Word or .bib file.

SciSpace would allow download of your references in Current Hypertension Reviews Endnote style, according to bentham-science guidelines.

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