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Journal of Cellular Physiology — Template for authors

Publisher: Wiley

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Guideline source

Categories	Rank	Trend in last 3 yrs
Clinical Biochemistry	#12 of 113	up by 6 ranks
Physiology	#23 of 169	up by 10 ranks
Cell Biology	#51 of 279	up by 32 ranks

Journal quality:

High

Last 4 years overview: 4033 Published Papers | 35913 Citations

Indexed in: Scopus

Last updated: 07/06/2020

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General info

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SNIP: 1.002

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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.

5.546

23% from 2018

Impact factor for Journal of Cellular Physiology from 2016 - 2019
Year	Value
2019	5.546
2018	4.522
2017	3.923
2016	4.08

Graph view

8.9

71% from 2019

CiteRatio for Journal of Cellular Physiology from 2016 - 2020
Year	Value
2020	8.9
2019	5.2
2018	5.8
2017	7.0
2016	7.6

Graph view

Insights

Impact factor of this journal has increased by 23% in last year.
This journal’s impact factor is in the top 10 percentile category.

Insights

CiteRatio of this journal has increased by 71% 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.

1.529

21% from 2019

SJR for Journal of Cellular Physiology from 2016 - 2020
Year	Value
2020	1.529
2019	1.267
2018	1.445
2017	1.641
2016	1.767

Graph view

1.245

5% from 2019

SNIP for Journal of Cellular Physiology from 2016 - 2020
Year	Value
2020	1.245
2019	1.186
2018	1.094
2017	1.024
2016	1.046

Graph view

Insights

SJR of this journal has increased by 21% in last years.
This journal’s SJR is in the top 10 percentile category.

Insights

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

Journal of Cellular Physiology

Guideline source: View

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Wiley

Journal of Cellular Physiology

The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal. Read Less

Clinical Biochemistry

Physiology

Cell Biology

Biochemistry, Genetics and Molecular Biology

Last updated on	07 Jun 2020
ISSN	0021-9541
Impact Factor	High - 1.117
Open Access	Yes
Sherpa RoMEO Archiving Policy	Yellow
Plagiarism Check	Available via Turnitin
Endnote Style	Download Available
Bibliography Name	apa
Citation Type	Author Year (Blonder et al. 1982)
Bibliography Example	Blonder, G. E., Tinkham, M., & Klapwijk, T. M. (1982). Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B, 25(7), 4515–4532.

Top papers written in this journal

Journal Article • DOI: 10.1002/(SICI)1097-4652(200003)182:3<311::AID-JCP1>3.0.CO;2-9 •

The Ki‐67 protein: From the known and the unknown

Thomas Scholzen, Johannes Gerdes

01 Mar 2000 - Journal of Cellular Physiology

Abstract:

The expression of the human Ki-67 protein is strictly associated with cell proliferation. During interphase, the antigen can be exclusively detected within the nucleus, whereas in mitosis most of the protein is relocated to the surface of the chromosomes. The fact that the Ki-67 protein is present during all active phases of ... The expression of the human Ki-67 protein is strictly associated with cell proliferation. During interphase, the antigen can be exclusively detected within the nucleus, whereas in mitosis most of the protein is relocated to the surface of the chromosomes. The fact that the Ki-67 protein is present during all active phases of the cell cycle (G(1), S, G(2), and mitosis), but is absent from resting cells (G(0)), makes it an excellent marker for determining the so-called growth fraction of a given cell population. In the first part of this study, the term proliferation marker is discussed and examples of the applications of anti-Ki-67 protein antibodies in diagnostics of human tumors are given. The fraction of Ki-67-positive tumor cells (the Ki-67 labeling index) is often correlated with the clinical course of the disease. The best-studied examples in this context are carcinomas of the prostate and the breast. For these types of tumors, the prognostic value for survival and tumor recurrence has repeatedly been proven in uni- and multivariate analysis. The preparation of new monoclonal antibodies that react with the Ki-67 equivalent protein from rodents now extends the use of the Ki-67 protein as a proliferation marker to laboratory animals that are routinely used in basic research. The second part of this review focuses on the biology of the Ki-67 protein. Our current knowledge of the Ki-67 gene and protein structure, mRNA splicing, expression, and cellular localization during the cell-division cycle is summarized and discussed. Although the Ki-67 protein is well characterized on the molecular level and extensively used as a proliferation marker, the functional significance still remains unclear. There are indications, however, that Ki-67 protein expression is an absolute requirement for progression through the cell-division cycle. read more

Topics:

Retinoblastoma-like protein 1 (66%)66% related to the paper, Ki-67 (63%)63% related to the paper, Proliferation Marker (60%)60% related to the paper,

4,359 Citations

Open access • Journal Article • DOI: 10.1002/JCP.10119 •

Cellular response to oxidative stress: signaling for suicide and survival.

Jennifer L. Martindale¹, Nikki J. Holbrook¹, •

01 Jul 2002 - Journal of Cellular Physiology

Abstract:

Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The importance of oxidative damage to the pathogenesis of ma... Reactive oxygen species (ROS), whether produced endogenously as a consequence of normal cell functions or derived from external sources, pose a constant threat to cells living in an aerobic environment as they can result in severe damage to DNA, protein, and lipids. The importance of oxidative damage to the pathogenesis of many diseases as well as to degenerative processes of aging has becoming increasingly apparent over the past few years. Cells contain a number of antioxidant defenses to minimize fluctuations in ROS, but ROS generation often exceeds the cell's antioxidant capacity, resulting in a condition termed oxidative stress. Host survival depends upon the ability of cells and tissues to adapt to or resist the stress, and repair or remove damaged molecules or cells. Numerous stress response mechanisms have evolved for these purposes, and they are rapidly activated in response to oxidative insults. Some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death. Still others have been implicated in both extremes depending on the particular circumstances. In this review, we discuss the various signaling pathways known to be activated in response to oxidative stress in mammalian cells, the mechanisms leading to their activation, and their roles in influencing cell survival. These pathways constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or attenuating its sequelae. read more

Topics:

Oxidative stress (57%)57% related to the paper

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2,222 Citations

Journal Article • DOI: 10.1002/JCP.1040910303 •

Conditions controlling the proliferation of haemopoietic stem cells in vitro.

T. M. Dexter, T. D. Allen,

01 Jun 1977 - Journal of Cellular Physiology

Abstract:

A liquid culture system is described whereby proliferation of haemopoietic stem cells (CFU-S), production of granulocyte precursor cells (CFU-C), and extensive granulopoiesis can be maintained in vitro for several months. Such cultures consist of adherent and non-adherent populations of cells. The adherent population contains... A liquid culture system is described whereby proliferation of haemopoietic stem cells (CFU-S), production of granulocyte precursor cells (CFU-C), and extensive granulopoiesis can be maintained in vitro for several months. Such cultures consist of adherent and non-adherent populations of cells. The adherent population contains phagocytic mononuclear cells, “epithelial” cells, and “giant fat” cells. The latter appear to be particularly important for stem cell maintenance and furthermore there is a strong tendency for maturing granulocytes to selectively cluster in and around areas of “giant fat” cell aggregations. By “feeding” the cultures at weekly intervals, between 10 to 15 “population doublings” of functionally normal CFU-S regularly occurs. Increased “population doublings” may be obtained by feeding twice weekly. The cultures show initially extensive granulopoiesis followed, in a majority of cases, by an accumulation of blast cells. Eventually both blast cells and granulocytes decline and the cultures contain predominantly phagocytic mononuclear cells. Culturing at 33°C leads to the development of a more profuse growth of adherent cells and these cultures show better maintenance of stem cells and increased cell density. When tested for colony stimulating activity (CSA) the cultures were uniformly negative. Addition of exogenous CSA caused a rapid decline in stem cells, reduced granulopoiesis and an accumulation of phagocytic mononuclear cells. read more

Topics:

Granulopoiesis (61%)61% related to the paper, Stem cell (61%)61% related to the paper, Granulocyte Precursor Cells (56%)56% related to the paper,

2,178 Citations

Journal Article • DOI: 10.1002/JCP.26429 •

Macrophage plasticity, polarization, and function in health and disease.

Abbas Shapouri-Moghaddam, Saeed Mohammadian, •

01 Sep 2018 - Journal of Cellular Physiology

Abstract:

Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytoki... Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytokines such as IFN-γ, GM-CSF, and produce pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α; and 2) Alternatively activated or M2 macrophages, which are anti-inflammatory and immunoregulatory and polarized by Th2 cytokines such as IL-4 and IL-13 and produce anti-inflammatory cytokines such as IL-10 and TGF-β. M1 and M2 macrophages have different functions and transcriptional profiles. They have unique abilities by destroying pathogens or repair the inflammation-associated injury. It is known that M1/M2 macrophage balance polarization governs the fate of an organ in inflammation or injury. When the infection or inflammation is severe enough to affect an organ, macrophages first exhibit the M1 phenotype to release TNF-α, IL-1β, IL-12, and IL-23 against the stimulus. But, if M1 phase continues, it can cause tissue damage. Therefore, M2 macrophages secrete high amounts of IL-10 and TGF-β to suppress the inflammation, contribute to tissue repair, remodeling, vasculogenesis, and retain homeostasis. In this review, we first discuss the basic biology of macrophages including origin, differentiation and activation, tissue distribution, plasticity and polarization, migration, antigen presentation capacity, cytokine and chemokine production, metabolism, and involvement of microRNAs in macrophage polarization and function. Secondly, we discuss the protective and pathogenic role of the macrophage subsets in normal and pathological pregnancy, anti-microbial defense, anti-tumor immunity, metabolic disease and obesity, asthma and allergy, atherosclerosis, fibrosis, wound healing, and autoimmunity. read more

Topics:

Macrophage polarization (69%)69% related to the paper, M2 Macrophage (59%)59% related to the paper, Cytokine (57%)57% related to the paper,

2,176 Citations

Open access • Journal Article • DOI: 10.1002/JCP.21200 •

Adult mesenchymal stem cells for tissue engineering versus regenerative medicine.

Arnold I. Caplan¹ •

01 Nov 2007 - Journal of Cellular Physiology

Abstract:

Adult mesenchymal stem cells (MSCs) can be isolated from bone marrow or marrow aspirates and because they are culture-dish adherent, they can be expanded in culture while maintaining their multipotency. The MSCs have been used in preclinical models for tissue engineering of bone, cartilage, muscle, marrow stroma, tendon, fat,... Adult mesenchymal stem cells (MSCs) can be isolated from bone marrow or marrow aspirates and because they are culture-dish adherent, they can be expanded in culture while maintaining their multipotency. The MSCs have been used in preclinical models for tissue engineering of bone, cartilage, muscle, marrow stroma, tendon, fat, and other connective tissues. These tissue-engineered materials show considerable promise for use in rebuilding damaged or diseased mesenchymal tissues. Unanticipated is the realization that the MSCs secrete a large spectrum of bioactive molecules. These molecules are immunosuppressive, especially for T-cells and, thus, allogeneic MSCs can be considered for therapeutic use. In this context, the secreted bioactive molecules provide a regenerative microenvironment for a variety of injured adult tissues to limit the area of damage and to mount a self-regulated regenerative response. This regenerative microenvironment is referred to as trophic activity and, therefore, MSCs appear to be valuable mediators for tissue repair and regeneration. The natural titers of MSCs that are drawn to sites of tissue injury can be augmented by allogeneic MSCs delivered via the bloodstream. Indeed, human clinical trials are now under way to use allogeneic MSCs for treatment of myocardial infarcts, graft-versus-host disease, Crohn's Disease, cartilage and meniscus repair, stroke, and spinal cord injury. This review summarizes the biological basis for the in vivo functioning of MSCs through development and aging. read more

Topics:

Stem cell transplantation for articular cartilage repair (66%)66% related to the paper, Clinical uses of mesenchymal stem cells (62%)62% related to the paper, Mesenchymal stem cell (57%)57% related to the paper,

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1,886 Citations

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3. Can I cite my article in multiple styles in Journal of Cellular Physiology?

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After writing your paper autoformatting in Journal of Cellular Physiology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Journal of Cellular Physiology'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 Journal of Cellular Physiology?

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 Journal of Cellular Physiology. 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:

Pre-prints as being the version of the paper before peer review and
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 Journal of Cellular Physiology?

The 5 most common citation types in order of usage for Journal of Cellular Physiology are:.

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

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Journal of Cellular Physiology — Template for authors

Related Journals

Journal Performance & Insights

Impact Factor

CiteRatio

5.546

8.9

Insights

Insights

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

1.529

1.245

Insights

Insights

Journal of Cellular Physiology

Journal of Cellular Physiology

Top papers written in this journal

Abstract:

Topics:

Abstract:

Topics:

Abstract:

Topics:

Abstract:

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Abstract:

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What to expect from SciSpace?

Speed and accuracy over MS Word

Plagiarism Reports via Turnitin

Freedom from formatting guidelines

Easy support from all your favorite tools

Frequently asked questions

Fast and reliable, built for complaince.

No word template required

Verifed journal formats

Trusted by academicians

Fast and reliable,
built for complaince.