Example of Cardiovascular Toxicology format
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Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format
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Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format Example of Cardiovascular Toxicology format
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This content is only for preview purposes. The original open access content can be found here.
open access Open Access

Cardiovascular Toxicology — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Cardiology and Cardiovascular Medicine #76 of 317 up up by 19 ranks
Toxicology #49 of 122 -
Molecular Biology #213 of 382 down down by 5 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 235 Published Papers | 1117 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 06/07/2020
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FAQ

Related Journals

open access Open Access

Elsevier

Quality:  
High
CiteRatio: 7.0
SJR: 1.645
SNIP: 1.132
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SAGE

Quality:  
Good
CiteRatio: 3.0
SJR: 0.613
SNIP: 0.814
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Taylor and Francis

Quality:  
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CiteRatio: 15.1
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open access Open Access

Taylor and Francis

Quality:  
High
CiteRatio: 2.7
SJR: 0.422
SNIP: 0.671

Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

A measure of average citations received per peer-reviewed paper published in the journal.

2.284

13% from 2018

Impact factor for Cardiovascular Toxicology from 2016 - 2019
Year Value
2019 2.284
2018 2.63
2017 2.989
2016 2.712
graph view Graph view
table view Table view

4.8

7% from 2019

CiteRatio for Cardiovascular Toxicology from 2016 - 2020
Year Value
2020 4.8
2019 4.5
2018 4.6
2017 4.3
2016 4.4
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 13% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 7% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

0.723

2% from 2019

SJR for Cardiovascular Toxicology from 2016 - 2020
Year Value
2020 0.723
2019 0.706
2018 0.837
2017 0.836
2016 0.774
graph view Graph view
table view Table view

1.03

14% from 2019

SNIP for Cardiovascular Toxicology from 2016 - 2020
Year Value
2020 1.03
2019 0.9
2018 1.035
2017 0.912
2016 0.725
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 2% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 14% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Cardiovascular Toxicology

Guideline source: View

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Springer

Cardiovascular Toxicology

Cardiovascular Toxicology is the only journal dedicated to publishing contemporary issues, timely reviews, and experimental and clinical data on toxicological aspects of cardiovascular disease. CT publishes papers that will elucidate the effects, molecular mechanisms, and sign...... Read More

Medicine

i
Last updated on
06 Jul 2020
i
ISSN
1606-8610
i
Impact Factor
Medium - 0.943
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
White faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
SPBASIC
i
Citation Type
Author Year
(Blonder et al, 1982)
i
Bibliography Example
Beenakker CWJ (2006) Specular andreev reflection in graphene. Phys Rev Lett 97(6):067,007, URL 10.1103/PhysRevLett.97.067007

Top papers written in this journal

Journal Article DOI: 10.1385/CT:6:2:111
The NF-kappaB regulatory network.
Allan R. Brasier1

Abstract:

Nuclear factor (NF)-κB is a family of seven structurally related transcription factors that play a central role in cardiovascular growth, stress response, and inflammation by controlling gene network expression. Although the NF-κB subunits are ubiquitously expressed, their actions are regulated in a cell-type and stimulus-spe... Nuclear factor (NF)-κB is a family of seven structurally related transcription factors that play a central role in cardiovascular growth, stress response, and inflammation by controlling gene network expression. Although the NF-κB subunits are ubiquitously expressed, their actions are regulated in a cell-type and stimulus-specific manner, allowing for a diverse spectrum of effects. For example, NF-κB is activated by cytokines, reactive oxygen species, bacterial cell wall products, vasopressors, viral infection, and DNA damage. Recent molecular dissection of its mechanisms for activation has shown that NF-κB can be induced by the so-called “canonical” and “noncanonical” pathways, leading to distinct patterns in the individual subunits activated and down-stream genetic responses produced. The canonical pathway involves activating the IκB kinase (IKK) with subsequent phosphorylation-induced proteolysis of the IκBα inhibitors and consequent nuclear translocation of the Rel A transcriptional activator. Recent work using high-density oligonucleotide arrays have begun to systematically dissect the scope of the gene network under canonical NF-κB control and have yielded important insights into biological pathways controlled by it. This pathway controls expression of noncontiguous, functionally discrete groups of genes (“regulons”), whose temporal expression occurs in waves. Moreover, its mode of activation (oscillatory or monophasic) plays an important role in determining the spectrum of target genes expressed. By contrast, the noncanonical NF-κB activation pathway involves activating the NF-κB inducing kinase (NIK) to stimulate IKKα-induced phosphorylation and proteolytic processing of the 100-kDa cytoplasmic NF-κB2 precursor. Activated NF-κB2 then forms a complex with Rel B and NIK to translocate into the nucleus thereby activating a distinct set of genes. Although the noncanonical pathway has been most clearly linked to control of adaptive immunity, recent intriguing studies have implicated this pathway in viral induced stress response and in the metabolic syndrome. In this way, a single family of transcription factors can respond to diverse stimuli to regulate cardiovascular homeostasis. read more read less

Topics:

Biological pathway (56%)56% related to the paper, Transcription factor (53%)53% related to the paper, IκB kinase (53%)53% related to the paper, IκBα (53%)53% related to the paper, Gene regulatory network (51%)51% related to the paper
506 Citations
Journal Article DOI: 10.1385/CT:1:3:181
Oxidative stress and diabetic cardiomyopathy: a brief review.
Lu Cai1, Y J Kang1, Y J Kang2

Abstract:

Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. Howe... Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. However, hyperglycemia, as an independent risk factor, directly causes cardiac damage and leads to diabetic cardiomyopathy. Diabetic cardiomyopathy can occur independent of vascular disease, although the mechanisms are largely unknown. Previous studies have paid little attention to the direct effects of hyperglycemia on cardiac myocytes, and most studies, especially in vitro, have mainly focused on the molecular mechanisms underlying pathogenic alterations in vascular smooth-muscle cells and endothelial cells. Thus, a comprehensive understanding of the mechanisms of diabetic cardiomyopathy is urgently needed to develop approaches for the prevention and treatment of diabetic cardiac complications. This review provides a survey of current understanding of diabetic cardiomyopathy. Current consensus is that hyperglycemia results in the production of reactive oxygen and nitrogen species, which leads to oxidative myocardial injury. Alterations in myocardial structure and function occur in the late stage of diabetes. These chronic alterations are believed to result from acute cardiac responses to suddenly increased glucose levels at the early stage of diabetes. Oxidative stress, induced by reactive oxygen and nitrogen species derived from hyperglycemia, causes abnormal gene expression, altered signal transduction, and the activation of pathways leading to programmed myocardial cell deaths. The resulting myocardial cell loss thus plays a critical role in the development of diabetic cardiomyopathy. Advances in the application of various strategies for targeting the prevention of hyperglycemia-induced oxidative myocardial injury may be fruitful. read more read less

Topics:

Diabetic cardiomyopathy (63%)63% related to the paper, Cardiomyopathy (62%)62% related to the paper, Diabetes mellitus (55%)55% related to the paper, Heart disease (54%)54% related to the paper, Oxidative stress (52%)52% related to the paper
339 Citations
Journal Article DOI: 10.1007/S12012-007-0015-3
Role of anthracyclines in the era of targeted therapy

Abstract:

Anthracyclines such as doxorubicin, epirubicin, and daunorubicin are among the most active cytoxic agents for treatment of a wide variety of solid tumors and hematological malignancies. The downside associated with chronic administration of anthracyclines is the induction of cardiomyopathy and congestive heart failure, usuall... Anthracyclines such as doxorubicin, epirubicin, and daunorubicin are among the most active cytoxic agents for treatment of a wide variety of solid tumors and hematological malignancies. The downside associated with chronic administration of anthracyclines is the induction of cardiomyopathy and congestive heart failure, usually refractory to common treatments. Anthracycline liposomal formulations are currently the best-known alternatives to improve the index and spectrum of anticancer activity of these drugs and decrease their cardiotoxicity. In the current target therapy era in oncology, anthracyclines increase the antitumor effects in more than additive fashion, being excellent partners for other active agents like taxanes and trastuzumab. It is important to note, however, that the enhanced antitumor activity of these combination therapies is often accompanied with increased cardiotoxicity. The issue of anthracycline cardiotoxicity has not been solved so far and it is also important to stress the current lack of proper prevention and treatment strategies. read more read less

Topics:

Anthracycline (60%)60% related to the paper, Cardiotoxicity (58%)58% related to the paper, Doxorubicin (58%)58% related to the paper, Daunorubicin (52%)52% related to the paper, Epirubicin (50%)50% related to the paper
250 Citations
Journal Article DOI: 10.1007/S12012-007-0008-2
Adriamycin-induced interference with cardiac mitochondrial calcium homeostasis.
Kendall B. Wallace1

Abstract:

Adriamycin (doxorubicin) is a potent and broad-spectrum antineoplastic agent, the clinical utility of which is limited by the development of a cumulative and irreversible cardiomyopathy. Although the drug affects numerous structures in different cell types, the mitochondrion appears to a principal subcellular target for the d... Adriamycin (doxorubicin) is a potent and broad-spectrum antineoplastic agent, the clinical utility of which is limited by the development of a cumulative and irreversible cardiomyopathy. Although the drug affects numerous structures in different cell types, the mitochondrion appears to a principal subcellular target for the development of cardiomyopathy. This review describes evidence demonstrating that adriamycin redox cycles on complex I of the mitochondrial electron transport chain to liberate highly reactive free radical species of molecular oxygen. The primary effect of adriamycin on mitochondrial performance is the interference with oxidative phosphorylation and inhibition of ATP synthesis. Free radicals liberated from adriamycin redox cycling are thought to be responsible for many of the secondary effects of adriamycin, including lipid peroxidation, the oxidation of both proteins and DNA, and the depletion of glutathione and pyridine nucleotide reducing equivalents in the cell. It is this altered redox status that is believed to cause assorted changes in intracellular regulation, including the induction of the mitochondrial permeability transition and complete loss of mitochondrial integrity and function. Associated with this is the interference with mitochondrial-mediated cell calcium signaling, which is implicated as essential to the capacity of mitochondria to participate in bioenergetic regulation in response to external signals reflecting changes in metabolic demand. If taken to an extreme, this loss of mitochondrial plasticity may manifest in the liberation of signals mediating either oncotic or necrotic cell death, further perpetuating the cardiac failure associated with adriamycin-induced mitochondrial cardiomyopathy. read more read less

Topics:

Mitochondrial permeability transition pore (61%)61% related to the paper, Mitochondrion (59%)59% related to the paper, Oxidative phosphorylation (54%)54% related to the paper, Intracellular (51%)51% related to the paper, Lipid peroxidation (50%)50% related to the paper
207 Citations
Journal Article DOI: 10.1385/CT:3:3:219
Cell death and diabetic cardiomyopathy.
Lu Cai1, Yujian Kang1

Abstract:

Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of di... Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of diabetic patients and antimal models; however, its importance in the development of diabetic cardiomyopathy is not completely understood. The goal of this review is to summarize our current understanding of the characteristics of diabetes-induced myocardial cell death. In the search of themechanisms by which diabetes induces myocardial cell death, multiple cell death pathways have been proposed. Reactive oxygen and nitrogen species accumulation plays a critical role in the cell death by antioxidants or inhibitors for apoptosis-specific signaling pathways results in a significant prevention of diabetic cardiotoxicity, suggesting that cell death in diabetic subjects plays an important role in the development of diabetic cardiomyopathy. read more read less

Topics:

Diabetic cardiomyopathy (56%)56% related to the paper, Diabetes mellitus (51%)51% related to the paper
176 Citations
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Frequently asked questions

1. Can I write Cardiovascular Toxicology in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Cardiovascular Toxicology guidelines and auto format it.

2. Do you follow the Cardiovascular Toxicology guidelines?

Yes, the template is compliant with the Cardiovascular Toxicology guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Cardiovascular Toxicology?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Cardiovascular Toxicology citation style.

4. Can I use the Cardiovascular Toxicology templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Cardiovascular Toxicology.

5. Can I use a manuscript in Cardiovascular Toxicology that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Cardiovascular Toxicology that you can download at the end.

6. How long does it usually take you to format my papers in Cardiovascular Toxicology?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in Cardiovascular Toxicology.

7. Where can I find the template for the Cardiovascular Toxicology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Cardiovascular Toxicology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the Cardiovascular Toxicology's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. Cardiovascular Toxicology an online tool or is there a desktop version?

SciSpace's Cardiovascular Toxicology is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like Cardiovascular Toxicology?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like Cardiovascular Toxicology?”

11. What is the output that I would get after using Cardiovascular Toxicology?

After writing your paper autoformatting in Cardiovascular Toxicology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Cardiovascular Toxicology's impact factor high enough that I should try publishing my article there?

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 these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Cardiovascular Toxicology?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Cardiovascular Toxicology. The table below indicates the level of access a journal has as per Sherpa Romeo's 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.

14. What are the most common citation types In Cardiovascular Toxicology?

The 5 most common citation types in order of usage for Cardiovascular Toxicology are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

15. How do I submit my article to the Cardiovascular Toxicology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Cardiovascular Toxicology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Cardiovascular Toxicology in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Cardiovascular Toxicology Endnote style according to Elsevier guidelines.

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