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GSK3 as a Master Regulator of Cellular Processes, 2nd Edition
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GSK3 as a Master Regulator of Cellular Processes, 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 November 2024) | Viewed by 2595

Special Issue Editors

Prof. Dr. Ralf Lichtinghagen

E-Mail Website
Guest Editor
Institute of Clinical Chemistry, Hannover Medical School, 30625 Hannover, Germany
Interests: molecular diagnostics; blood sampling; biomarkers; cytokines; hormones; MMP; inflammation; fibrosis; stroke
Special Issues, Collections and Topics in MDPI journals
Dr. René Huber

E-Mail Website
Guest Editor
Institute of Clinical Chemistry, Hannover Medical School, 30625 Hannover, Germanyny
Interests: monocyte/macrophages; resolution of inflammation; TNF; signal transduction; GSK3; transcriptional regulation; NF-κB; AP-1; rheumatoid arthritis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glycogen synthase kinase (GSK) 3α and β are key proteins targeting a plethora of molecules and regulating various cellular processes thus steering central functions such as metabolism, proliferation, differentiation, apoptosis, adhesion, and migration. In consequence, GSK3 activity has to be tightly controlled to ensure the regulated course of cellular development and behavior whilst dysregulations may result in a variety of disorders such as neurological/neurodegenerative, metabolic, and inflammatory diseases, or different forms of cancer. Decades of research provided profound knowledge on the activity, regulation, and function of the GSK3 paralogues during physiological as well as pathophysiological events. In many biological contexts, however, GSK3 appears to mediate unexpected, in part even conflicting effects. Thus, its specific behavior in a particular situation (e.g., during infections or cancer) is often difficult to predict and its role is still controversially discussed. This Special Issue aims at further elucidating the modulation of GSK3α and β under various conditions and their role in controlling multiple processes within the cell. We cordially invite you to submit a respective manuscript; all types of papers (research articles, brief reports, reviews, hypotheses, case reports, communications) are welcome.

More published papers could be found in the closed Special Issue: GSK3 as a Master Regulator of Cellular Processes

Prof. Dr. Ralf Lichtinghagen
Dr. René Huber
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • GSK3α
  • GSK3β
  • signal transduction
  • gene regulation
  • metabolism
  • proliferation
  • differentiation
  • apoptosis
  • migration
  • neurological and neurodegenerative diseases
  • cancer
  • inflammation

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Published Papers (2 papers)

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Research

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9 pages, 8828 KiB  
Article
Myeloid GSK3α Deficiency Reduces Lesional Inflammation and Neovascularization during Atherosclerotic Progression
by Sarvatit Patel, Nisarg Shah, Brooke D’Mello, Anson Lee and Geoff H. Werstuck
Int. J. Mol. Sci. 2024, 25(20), 10897; https://doi.org/10.3390/ijms252010897 - 10 Oct 2024
Viewed by 681
Abstract
The molecular mechanisms by which cardiovascular risk factors promote the development of atherosclerosis are poorly understood. We have recently shown that genetic ablation of myeloid glycogen synthase kinase (GSK)-3α attenuates atherosclerotic lesion development in low-density lipoprotein receptor-deficient (Ldlr−/−) mice. However, the [...] Read more.
The molecular mechanisms by which cardiovascular risk factors promote the development of atherosclerosis are poorly understood. We have recently shown that genetic ablation of myeloid glycogen synthase kinase (GSK)-3α attenuates atherosclerotic lesion development in low-density lipoprotein receptor-deficient (Ldlr−/−) mice. However, the precise contributions of GSK3α/β in atherogenesis are not known. The aim of this study is to investigate the effect of GSK3α and/or β deficiency on lesional inflammation and plaque vascularization. Five-week-old female Ldlr−/− mice were fed a high-fat diet for 10 weeks to establish atherosclerotic lesions. Mice were harvested at 15 weeks of age and atherosclerotic lesions were characterized. The results indicate that, in addition to significantly reducing plaque volume, GSK3α-deficiency decreases inflammation, reduces vasa vasorum density at the aortic sinus, and reduces plasma c-reactive protein (CRP) levels. GSK3β-deficiency is associated with decreased plasma CRP levels but does not affect lesional inflammation or vascularization. These results suggest GSK3α may be an applicable target for the development of novel anti-atherogenic therapies. Full article
(This article belongs to the Special Issue GSK3 as a Master Regulator of Cellular Processes, 2nd Edition)
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Review

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30 pages, 3301 KiB  
Review
GSK3-Driven Modulation of Inflammation and Tissue Integrity in the Animal Model
by Friederike Kühl, Korbinian Brand, Ralf Lichtinghagen and René Huber
Int. J. Mol. Sci. 2024, 25(15), 8263; https://doi.org/10.3390/ijms25158263 - 29 Jul 2024
Viewed by 1400
Abstract
Nowadays, GSK3 is accepted as an enzyme strongly involved in the regulation of inflammation by balancing the pro- and anti-inflammatory responses of cells and organisms, thus influencing the initiation, progression, and resolution of inflammatory processes at multiple levels. Disturbances within its broad functional [...] Read more.
Nowadays, GSK3 is accepted as an enzyme strongly involved in the regulation of inflammation by balancing the pro- and anti-inflammatory responses of cells and organisms, thus influencing the initiation, progression, and resolution of inflammatory processes at multiple levels. Disturbances within its broad functional scope, either intrinsically or extrinsically induced, harbor the risk of profound disruptions to the regular course of the immune response, including the formation of severe inflammation-related diseases. Therefore, this review aims at summarizing and contextualizing the current knowledge derived from animal models to further shape our understanding of GSK3α and β and their roles in the inflammatory process and the occurrence of tissue/organ damage. Following a short recapitulation of structure, function, and regulation of GSK3, we will focus on the lessons learned from GSK3α/β knock-out and knock-in/overexpression models, both conventional and conditional, as well as a variety of (predominantly rodent) disease models reflecting defined pathologic conditions with a significant proportion of inflammation and inflammation-related tissue injury. In summary, the literature suggests that GSK3 acts as a crucial switch driving pro-inflammatory and destructive processes and thus contributes significantly to the pathogenesis of inflammation-associated diseases. Full article
(This article belongs to the Special Issue GSK3 as a Master Regulator of Cellular Processes, 2nd Edition)
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