Example of Angiogenesis format
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Angiogenesis — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Clinical Biochemistry #2 of 113 up up by 3 ranks
Physiology #8 of 169 up up by 7 ranks
Cancer Research #16 of 207 up up by 14 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 198 Published Papers | 3099 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 18/07/2020
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Related Journals

open access Open Access

Wiley

Quality:  
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CiteRatio: 8.9
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SNIP: 1.245
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Taylor and Francis

Quality:  
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CiteRatio: 5.5
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open access Open Access

Taylor and Francis

Quality:  
High
CiteRatio: 6.2
SJR: 0.981
SNIP: 1.447
open access Open Access

SAGE

Quality:  
High
CiteRatio: 9.3
SJR: 1.055
SNIP: 0.903

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.

9.78

70% from 2018

Impact factor for Angiogenesis from 2016 - 2019
Year Value
2019 9.78
2018 5.759
2017 4.351
2016 5.253
graph view Graph view
table view Table view

15.7

37% from 2019

CiteRatio for Angiogenesis from 2016 - 2020
Year Value
2020 15.7
2019 11.5
2018 7.9
2017 9.8
2016 9.1
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 70% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 37% 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.

1.061

26% from 2019

SJR for Angiogenesis from 2016 - 2020
Year Value
2020 1.061
2019 0.839
2018 1.193
2017 2.177
2016 1.875
graph view Graph view
table view Table view

2.057

34% from 2019

SNIP for Angiogenesis from 2016 - 2020
Year Value
2020 2.057
2019 1.538
2018 1.252
2017 1.423
2016 1.254
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 26% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 34% in last years.
  • This journal’s SNIP is in the top 10 percentile category.
Angiogenesis

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Springer

Angiogenesis

Approved by publishing and review experts on SciSpace, this template is built as per for Angiogenesis formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 383 authors to write and format their manuscripts to this journal.

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Last updated on
18 Jul 2020
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ISSN
1573-7209
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Open Access
Hybrid
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Sherpa RoMEO Archiving Policy
Green faq
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Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Citation Type
Author Year
(Blonder et al, 1982)
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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

open accessOpen access Journal Article DOI: 10.1007/S10456-011-9249-6
Binding and neutralization of vascular endothelial growth factor (VEGF) and related ligands by VEGF Trap, ranibizumab and bevacizumab
03 Feb 2012 - Angiogenesis

Abstract:

Pharmacological inhibition of VEGF-A has proven to be effective in inhibiting angiogenesis and vascular leak associated with cancers and various eye diseases. However, little information is currently available on the binding kinetics and relative biological activity of various VEGF inhibitors. Therefore, we have evaluated the... Pharmacological inhibition of VEGF-A has proven to be effective in inhibiting angiogenesis and vascular leak associated with cancers and various eye diseases. However, little information is currently available on the binding kinetics and relative biological activity of various VEGF inhibitors. Therefore, we have evaluated the binding kinetics of two anti-VEGF antibodies, ranibizumab and bevacizumab, and VEGF Trap (also known as aflibercept), a novel type of soluble decoy receptor, with substantially higher affinity than conventional soluble VEGF receptors. VEGF Trap bound to all isoforms of human VEGF-A tested with subpicomolar affinity. Ranibizumab and bevacizumab also bound human VEGF-A, but with markedly lower affinity. The association rate for VEGF Trap binding to VEGF-A was orders of magnitude faster than that measured for bevacizumab and ranibizumab. Similarly, in cell-based bioassays, VEGF Trap inhibited the activation of VEGFR1 and VEGFR2, as well as VEGF-A induced calcium mobilization and migration in human endothelial cells more potently than ranibizumab or bevacizumab. Only VEGF Trap bound human PlGF and VEGF-B, and inhibited VEGFR1 activation and HUVEC migration induced by PlGF. These data differentiate VEGF Trap from ranibizumab and bevacizumab in terms of its markedly higher affinity for VEGF-A, as well as its ability to bind VEGF-B and PlGF. read more read less

Topics:

Vascular endothelial growth factor (60%)60% related to the paper, Ranibizumab (57%)57% related to the paper, Angiogenesis (50%)50% related to the paper
View PDF
858 Citations
Journal Article DOI: 10.1007/S10456-017-9562-9
Tumor angiogenesis and vascular normalization: alternative therapeutic targets.
Claire Viallard, Bruno Larrivée1
28 Jun 2017 - Angiogenesis

Abstract:

Tumor blood vessels are a key target for cancer therapeutic management. Tumor cells secrete high levels of pro-angiogenic factors which contribute to the creation of an abnormal vascular network characterized by disorganized, immature and permeable blood vessels, resulting in poorly perfused tumors. The hypoxic microenvironme... Tumor blood vessels are a key target for cancer therapeutic management. Tumor cells secrete high levels of pro-angiogenic factors which contribute to the creation of an abnormal vascular network characterized by disorganized, immature and permeable blood vessels, resulting in poorly perfused tumors. The hypoxic microenvironment created by impaired tumor perfusion can promote the selection of more invasive and aggressive tumor cells and can also impede the tumor-killing action of immune cells. Furthermore, abnormal tumor perfusion also reduces the diffusion of chemotherapeutic drugs and radiotherapy efficiency. To fight against this defective phenotype, the normalization of the tumor vasculature has emerged as a new therapeutic strategy. Vascular normalization, by restoring proper tumor perfusion and oxygenation, could limit tumor cell invasiveness and improve the effectiveness of anticancer treatments. In this review, we investigate the mechanisms involved in tumor angiogenesis and describe strategies used to achieve vascular normalization. read more read less

Topics:

Angiogenesis (55%)55% related to the paper
828 Citations
Journal Article DOI: 10.1007/S10456-013-9381-6
Anti-inflammatory M2, but not pro-inflammatory M1 macrophages promote angiogenesis in vivo
01 Jan 2014 - Angiogenesis

Abstract:

Objective Macrophages show extreme heterogeneity and different subsets have been characterized by their activation route and their function. For instance, macrophage subsets are distinct by acting differently under pathophysiological conditions such as inflammation and cancer. Macrophages also contribute to angiogenesis, but... Objective Macrophages show extreme heterogeneity and different subsets have been characterized by their activation route and their function. For instance, macrophage subsets are distinct by acting differently under pathophysiological conditions such as inflammation and cancer. Macrophages also contribute to angiogenesis, but the role of various specific subsets in angiogenesis has not been thoroughly investigated. read more read less

Topics:

Macrophage (53%)53% related to the paper, Angiogenesis (53%)53% related to the paper, Neovascularization (51%)51% related to the paper, Inflammation (51%)51% related to the paper
610 Citations
open accessOpen access Journal Article DOI: 10.1007/S10456-014-9420-Y
Anti-angiogenic therapy for cancer: current progress, unresolved questions and future directions
Naveen S. Vasudev1, Andrew R. Reynolds1
31 Jan 2014 - Angiogenesis

Abstract:

Tumours require a vascular supply to grow and can achieve this via the expression of pro-angiogenic growth factors, including members of the vascular endothelial growth factor (VEGF) family of ligands. Since one or more of the VEGF ligand family is overexpressed in most solid cancers, there was great optimism that inhibition ... Tumours require a vascular supply to grow and can achieve this via the expression of pro-angiogenic growth factors, including members of the vascular endothelial growth factor (VEGF) family of ligands. Since one or more of the VEGF ligand family is overexpressed in most solid cancers, there was great optimism that inhibition of the VEGF pathway would represent an effective anti-angiogenic therapy for most tumour types. Encouragingly, VEGF pathway targeted drugs such as bevacizumab, sunitinib and aflibercept have shown activity in certain settings. However, inhibition of VEGF signalling is not effective in all cancers, prompting the need to further understand how the vasculature can be effectively targeted in tumours. Here we present a succinct review of the progress with VEGF-targeted therapy and the unresolved questions that exist in the field: including its use in different disease stages (metastatic, adjuvant, neoadjuvant), interactions with chemotherapy, duration and scheduling of therapy, potential predictive biomarkers and proposed mechanisms of resistance, including paradoxical effects such as enhanced tumour aggressiveness. In terms of future directions, we discuss the need to delineate further the complexities of tumour vascularisation if we are to develop more effective and personalised anti-angiogenic therapies. read more read less

Topics:

Vascular endothelial growth factor (51%)51% related to the paper
View PDF
596 Citations
open accessOpen access Journal Article DOI: 10.1007/S10456-008-9099-Z
Vascular permeability, vascular hyperpermeability and angiogenesis
Janice A. Nagy1, Laura E. Benjamin1, Huiyan Zeng1, Ann M. Dvorak1, Harold F. Dvorak1
22 Feb 2008 - Angiogenesis

Abstract:

The vascular system has the critical function of supplying tissues with nutrients and clearing waste products. To accomplish these goals, the vasculature must be sufficiently permeable to allow the free, bidirectional passage of small molecules and gases and, to a lesser extent, of plasma proteins. Physiologists and many vasc... The vascular system has the critical function of supplying tissues with nutrients and clearing waste products. To accomplish these goals, the vasculature must be sufficiently permeable to allow the free, bidirectional passage of small molecules and gases and, to a lesser extent, of plasma proteins. Physiologists and many vascular biologists differ as to the definition of vascular permeability and the proper methodology for its measurement. We review these conflicting views, finding that both provide useful but complementary information. Vascular permeability by any measure is dramatically increased in acute and chronic inflammation, cancer, and wound healing. This hyperpermeability is mediated by acute or chronic exposure to vascular permeabilizing agents, particularly vascular permeability factor/vascular endothelial growth factor (VPF/VEGF, VEGF-A). We demonstrate that three distinctly different types of vascular permeability can be distinguished, based on the different types of microvessels involved, the composition of the extravasate, and the anatomic pathways by which molecules of different size cross-vascular endothelium. These are the basal vascular permeability (BVP) of normal tissues, the acute vascular hyperpermeability (AVH) that occurs in response to a single, brief exposure to VEGF-A or other vascular permeabilizing agents, and the chronic vascular hyperpermeability (CVH) that characterizes pathological angiogenesis. Finally, we list the numerous (at least 25) gene products that different authors have found to affect vascular permeability in variously engineered mice and classify them with respect to their participation, as far as possible, in BVP, AVH and CVH. Further work will be required to elucidate the signaling pathways by which each of these molecules, and others likely to be discovered, mediate the different types of vascular permeability. read more read less

Topics:

Vascular permeability (63%)63% related to the paper, Vascular endothelial growth factor (55%)55% related to the paper
View PDF
564 Citations
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Frequently asked questions

1. Can I write Angiogenesis in LaTeX?

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

2. Do you follow the Angiogenesis guidelines?

Yes, the template is compliant with the Angiogenesis 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 Angiogenesis?

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 Angiogenesis citation style.

4. Can I use the Angiogenesis 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 Angiogenesis.

5. Can I use a manuscript in Angiogenesis 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 Angiogenesis that you can download at the end.

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

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

7. Where can I find the template for the Angiogenesis?

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 Angiogenesis'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 Angiogenesis'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. Angiogenesis an online tool or is there a desktop version?

SciSpace's Angiogenesis 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 Angiogenesis?

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 Angiogenesis?”

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

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

12. Is Angiogenesis'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 Angiogenesis?

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 Angiogenesis. 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 Angiogenesis?

The 5 most common citation types in order of usage for Angiogenesis 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 Angiogenesis?

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 Angiogenesis's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Angiogenesis 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 Angiogenesis Endnote style according to Elsevier guidelines.

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I spent hours with MS word for reformatting. It was frustrating - plain and simple. With SciSpace, I can draft my manuscripts and once it is finished I can just submit. In case, I have to submit to another journal it is really just a button click instead of an afternoon of reformatting.

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