Example of Aging Cell format
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Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format Example of Aging Cell format
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Aging Cell — Template for authors

Publisher: Wiley
Categories Rank Trend in last 3 yrs
Aging #2 of 35 -
Cell Biology #34 of 279 down down by 8 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 688 Published Papers | 7957 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 29/06/2020
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Related Journals

open access Open Access

Elsevier

Quality:  
Good
CiteRatio: 6.2
SJR: 1.173
SNIP: 1.127
open access Open Access
recommended Recommended

Taylor and Francis

Quality:  
High
CiteRatio: 15.1
SJR: 3.934
SNIP: 2.351
open access Open Access

American Chemical Society

Quality:  
High
CiteRatio: 6.5
SJR: 1.158
SNIP: 1.002
open access Open Access

Nature

Quality:  
High
CiteRatio: 6.7
SJR: 1.542
SNIP: 1.216

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.

7.238

1% from 2018

Impact factor for Aging Cell from 2016 - 2019
Year Value
2019 7.238
2018 7.346
2017 7.627
2016 6.714
graph view Graph view
table view Table view

11.6

CiteRatio for Aging Cell from 2016 - 2020
Year Value
2020 11.6
2019 11.6
2018 12.2
2017 12.0
2016 12.1
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has decreased by 1% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • 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.

3.103

5% from 2019

SJR for Aging Cell from 2016 - 2020
Year Value
2020 3.103
2019 3.28
2018 3.809
2017 3.937
2016 4.053
graph view Graph view
table view Table view

1.713

9% from 2019

SNIP for Aging Cell from 2016 - 2020
Year Value
2020 1.713
2019 1.57
2018 1.583
2017 1.573
2016 1.415
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 5% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 9% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Aging Cell

Guideline source: View

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Wiley

Aging Cell

Aging Cell is the leading journal in geriatrics and gerontology and aims to publish novel and exciting science which addresses fundamental issues in the molecular biology of aging. All areas of aging biology are welcome in the journal and the experimental approaches used can b...... Read More

Ageing

Cell Biology

Biochemistry, Genetics and Molecular Biology

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Last updated on
29 Jun 2020
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ISSN
1474-9718
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Impact Factor
High - 1.409
i
Open Access
Yes
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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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Bibliography Name
apa
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Citation Type
Numbered
[25]
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Bibliography Example
Beenakker, C.W.J. (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: 10.1111/ACEL.12344
The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs
01 Aug 2015 - Aging Cell

Abstract:

The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous impact on quality of life and the burden of age-related chronic diseases. Here, we describe the rationale for identification and validation of a new class of drugs ter... The healthspan of mice is enhanced by killing senescent cells using a transgenic suicide gene. Achieving the same using small molecules would have a tremendous impact on quality of life and the burden of age-related chronic diseases. Here, we describe the rationale for identification and validation of a new class of drugs termed senolytics, which selectively kill senescent cells. By transcript analysis, we discovered increased expression of pro-survival networks in senescent cells, consistent with their established resistance to apoptosis. Using siRNA to silence expression of key nodes of this network, including ephrins (EFNB1 or 3), PI3Kδ, p21, BCL-xL, or plasminogen-activated inhibitor-2, killed senescent cells, but not proliferating or quiescent, differentiated cells. Drugs targeting these same factors selectively killed senescent cells. Dasatinib eliminated senescent human fat cell progenitors, while quercetin was more effective against senescent human endothelial cells and mouse BM-MSCs. The combination of dasatinib and quercetin was effective in eliminating senescent MEFs. In vivo, this combination reduced senescent cell burden in chronologically aged, radiation-exposed, and progeroid Ercc1(-/Δ) mice. In old mice, cardiac function and carotid vascular reactivity were improved 5 days after a single dose. Following irradiation of one limb in mice, a single dose led to improved exercise capacity for at least 7 months following drug treatment. Periodic drug administration extended healthspan in Ercc1(-/∆) mice, delaying age-related symptoms and pathology, osteoporosis, and loss of intervertebral disk proteoglycans. These results demonstrate the feasibility of selectively ablating senescent cells and the efficacy of senolytics for alleviating symptoms of frailty and extending healthspan. read more read less

Topics:

Senolytic (69%)69% related to the paper, Intervertebral disk (52%)52% related to the paper, Suicide gene (52%)52% related to the paper, Cellular differentiation (50%)50% related to the paper
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1,417 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1474-9726.2006.00199.X
Senescence‐associated β‐galactosidase is lysosomal β‐galactosidase
01 Apr 2006 - Aging Cell

Abstract:

Replicative senescence limits the proliferation of somatic cells passaged in culture and may reflect cellular aging in vivo. The most widely used biomarker for senescent and aging cells is senescence-associated beta-galactosidase (SA-beta-gal), which is defined as beta-galactosidase activity detectable at pH 6.0 in senescent ... Replicative senescence limits the proliferation of somatic cells passaged in culture and may reflect cellular aging in vivo. The most widely used biomarker for senescent and aging cells is senescence-associated beta-galactosidase (SA-beta-gal), which is defined as beta-galactosidase activity detectable at pH 6.0 in senescent cells, but the origin of SA-beta-gal and its cellular roles in senescence are not known. We demonstrate here that SA-beta-gal activity is expressed from GLB1, the gene encoding lysosomal beta-D-galactosidase, the activity of which is typically measured at acidic pH 4.5. Fibroblasts from patients with autosomal recessive G(M1)-gangliosidosis, which have defective lysosomal beta-galactosidase, did not express SA-beta-gal at late passages even though they underwent replicative senescence. In addition, late passage normal fibroblasts expressing small-hairpin interfering RNA that depleted GLB1 mRNA underwent senescence but failed to express SA-beta-gal. GLB1 mRNA depletion also prevented expression of SA-beta-gal activity in HeLa cervical carcinoma cells induced to enter a senescent state by repression of their endogenous human papillomavirus E7 oncogene. SA-beta-gal induction during senescence was due at least in part to increased expression of the lysosomal beta-galactosidase protein. These results also indicate that SA-beta-gal is not required for senescence. read more read less

Topics:

Senescence (61%)61% related to the paper, Cell aging (56%)56% related to the paper, Endogeny (52%)52% related to the paper, Gene expression (51%)51% related to the paper
905 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1474-9726.2010.00608.X
Fat tissue, aging, and cellular senescence
01 Oct 2010 - Aging Cell

Abstract:

Fat tissue, frequently the largest organ in humans, is at the nexus of mechanisms involved in longevity and age-related metabolic dysfunction. Fat distribution and function change dramatically throughout life. Obesity is associated with accelerated onset of diseases common in old age, while fat ablation and certain mutations ... Fat tissue, frequently the largest organ in humans, is at the nexus of mechanisms involved in longevity and age-related metabolic dysfunction. Fat distribution and function change dramatically throughout life. Obesity is associated with accelerated onset of diseases common in old age, while fat ablation and certain mutations affecting fat increase life span. Fat cells turn over throughout the life span. Fat cell progenitors, preadipocytes, are abundant, closely related to macrophages, and dysdifferentiate in old age, switching into a pro-inflammatory, tissue-remodeling, senescent-like state. Other mesenchymal progenitors also can acquire a pro-inflammatory, adipocyte-like phenotype with aging. We propose a hypothetical model in which cellular stress and preadipocyte overutilization with aging induce cellular senescence, leading to impaired adipogenesis, failure to sequester lipotoxic fatty acids, inflammatory cytokine and chemokine generation, and innate and adaptive immune response activation. These pro-inflammatory processes may amplify each other and have systemic consequences. This model is consistent with recent concepts about cellular senescence as a stress-responsive, adaptive phenotype that develops through multiple stages, including major metabolic and secretory readjustments, which can spread from cell to cell and can occur at any point during life. Senescence could be an alternative cell fate that develops in response to injury or metabolic dysfunction and might occur in nondividing as well as dividing cells. Consistent with this, a senescent-like state can develop in preadipocytes and fat cells from young obese individuals. Senescent, pro-inflammatory cells in fat could have profound clinical consequences because of the large size of the fat organ and its central metabolic role. read more read less

Topics:

Cell aging (60%)60% related to the paper, Senescence (59%)59% related to the paper, Adipose tissue (54%)54% related to the paper, Adipogenesis (51%)51% related to the paper
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883 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1474-9726.2006.00267.X
Lifespan extension by conditions that inhibit translation in Caenorhabditis elegans
Malene Hansen1, Stefan Taubert1, Douglas Crawford, Nataliya Libina, Seung-Jae Lee, Cynthia Kenyon
01 Feb 2007 - Aging Cell

Abstract:

Summary Many conditions that shift cells from states of nutrient utilization and growth to states of cell maintenance extend lifespan. We have carried out a systematic lifespan analysis of conditions that inhibit protein synthesis. We find that reducing the levels of ribosomal proteins, ribosomal-protein S6 kinase or transla... Summary Many conditions that shift cells from states of nutrient utilization and growth to states of cell maintenance extend lifespan. We have carried out a systematic lifespan analysis of conditions that inhibit protein synthesis. We find that reducing the levels of ribosomal proteins, ribosomal-protein S6 kinase or translation-initiation factors increases the lifespan of Caenorhabditis elegans. These perturbations, as well as inhibition of the nutrient sensor target of rapamycin (TOR), which is known to increase lifespan, all increase thermal-stress resistance. Thus inhibiting translation may extend lifespan by shifting cells to physiological states that favor maintenance and repair. Interestingly, different types of translation inhibition lead to one of two mutually exclusive outputs, one that increases lifespan and stress resistance through the transcription factor DAF-16/FOXO, and one that increases lifespan and stress resistance independently of DAF-16. Our findings link TOR, but not sir-2.1, to the longevity response induced by dietary restriction (DR) in C. elegans, and they suggest that neither TOR inhibition nor DR extends lifespan simply by reducing protein synthesis. read more read less
836 Citations
open accessOpen access Journal Article DOI: 10.1111/J.1474-9728.2004.00127.X
Aging activates adipogenic and suppresses osteogenic programs in mesenchymal marrow stroma/stem cells: the role of PPAR-γ2 transcription factor and TGF-β/BMP signaling pathways
Elena J. Moerman1, Kui Teng1, David A. Lipschitz1, Beata Lecka-Czernik1
01 Dec 2004 - Aging Cell

Abstract:

Osteoblasts and adipocytes originate from a common progenitor, which arises from bone marrow mesenchymal stroma/stem cells (mMSC). Aging causes a decrease in the number of bone-forming osteoblasts and an increase in the number of marrow adipocytes. Here, we demonstrate that, during aging, the status of mMSC changes with respe... Osteoblasts and adipocytes originate from a common progenitor, which arises from bone marrow mesenchymal stroma/stem cells (mMSC). Aging causes a decrease in the number of bone-forming osteoblasts and an increase in the number of marrow adipocytes. Here, we demonstrate that, during aging, the status of mMSC changes with respect to both their intrinsic differentiation potential and production of signaling molecules, which contributes to the formation of a specific marrow microenvironment necessary for maintenance of bone homeostasis. Aging causes a decrease in the commitment of mMSC to the osteoblast lineage and an increase in the commitment to the adipocyte lineage. This is reflected by changes in the expression of phenotype-specific gene markers. The expression of osteoblast-specific transcription factors, Runx2 and Dlx5, and osteoblast markers, collagen and osteocalcin, is decreased in aged mMSC. Conversely, the expression of adipocyte-specific transcription factor PPAR-γ2, shown previously to regulate osteoblast development and bone formation negatively and to regulate marrow adipocyte differentiation positively, is increased, as is a gene marker of adipocyte phenotype, fatty acid binding protein aP2. Furthermore, production of an endogeneous PPAR-γ activator(s) that stimulates adipocyte differentiation and production of autocrine/paracrine factor(s) that suppresses the osteoblastic phenotype are also increased. In addition, expression of different components of TGF-β and BMP2/4 signaling pathways is altered, suggesting that activities of these two cytokines essential for bone homeostasis change with aging. read more read less

Topics:

RUNX2 (60%)60% related to the paper, Osteoblast (60%)60% related to the paper, Paracrine signalling (58%)58% related to the paper, Cellular differentiation (57%)57% related to the paper, Cell aging (55%)55% related to the paper
733 Citations
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Aging Cell format uses apa citation style.

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Frequently asked questions

1. Can I write Aging Cell in LaTeX?

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

2. Do you follow the Aging Cell guidelines?

Yes, the template is compliant with the Aging Cell 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 Aging Cell?

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 Aging Cell citation style.

4. Can I use the Aging Cell 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 Aging Cell.

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

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

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

7. Where can I find the template for the Aging Cell?

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

SciSpace's Aging Cell 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 Aging Cell?

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 Aging Cell?”

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

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

12. Is Aging Cell'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 Aging Cell?

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 Aging Cell. 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 Aging Cell?

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

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

16. Can I download Aging Cell 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 Aging Cell Endnote style according to Elsevier guidelines.

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