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Protein Kinases in Metabolic Disorders
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Protein Kinases in Metabolic Disorders

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

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 7710

Special Issue Editors

Prof. Dr. Maria Ruzzene

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padova, Padova, Italy
Interests: signal transduction; cell signaling; signaling pathways; protein phosphorylation; protein kinases; protein phosphatases; protein kinase inhibitors; cancer biology; proteins; apoptosis; cell death; cancer research; cancer cell line
Special Issues, Collections and Topics in MDPI journals
Dr. Christian Borgo

E-Mail Website
Guest Editor
Department of Biomedical Sciences, University of Padova, Via U. Bassi 58/B, 35131 Padova, Italy
Interests: chronic myeloid leukemia; cystic fibrosis; glucose metabolism; drug-resistance; phosphorylation; protein kinase inhibitors; protein kinase ck2; CFTR
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim and scope of this Special Issue is to create a dedicated space for original research papers or reviews on the aberrant signaling of protein kinases involved in sustaining the development of metabolic disorders. The issue will include both metabolic diseases with genetic origin (such as Gaucher disease and familial hypercholesterolemia) and those of non-genetic origin (such as diabetes, fatty liver disease, metabolic syndrome). It will also be possible to consider papers on protein kinases involved in obesity and obesity-related metabolic diseases.

Prof. Dr. Maria Ruzzene
Dr. Christian Borgo
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

  • metabolic disorder
  • protein kinase
  • aberrant signaling
  • diabetes
  • obesity
  • altered metabolism

Published Papers (2 papers)

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Research

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16 pages, 2402 KiB  
Article
Chronic and Intermittent Hyperglycemia Modulates Expression of Key Molecules of PI3K/AKT Pathway in Differentiating Human Visceral Adipocytes
by Ewa Świderska, Justyna Strycharz, Adam Wróblewski, Piotr Czarny, Janusz Szemraj, Józef Drzewoski and Agnieszka Śliwińska
Int. J. Mol. Sci. 2021, 22(14), 7712; https://doi.org/10.3390/ijms22147712 - 19 Jul 2021
Cited by 4 | Viewed by 2492
Abstract
Background: Due to its prominence in the regulation of metabolism and inflammation, adipose tissue is a major target to investigate alterations in insulin action. This hormone activates PI3K/AKT pathway which is essential for glucose homeostasis, cell differentiation, and proliferation in insulin-sensitive tissues, like [...] Read more.
Background: Due to its prominence in the regulation of metabolism and inflammation, adipose tissue is a major target to investigate alterations in insulin action. This hormone activates PI3K/AKT pathway which is essential for glucose homeostasis, cell differentiation, and proliferation in insulin-sensitive tissues, like adipose tissue. The aim of this work was to evaluate the impact of chronic and intermittent high glucose on the expression of biomolecules of insulin signaling pathway during the differentiation and maturation of human visceral preadipocytes. Methods: Human visceral preadipocytes (HPA-V) cells were treated with high glucose (30 mM)during the proliferation and/or differentiation and/or maturation stage. The level of mRNA (by Real-Time PCR) and protein (by Elisa tests) expression of IRS1, PI3K, PTEN, AKT2, and GLUT4 was examined after each culture stage. Furthermore, we investigated whether miR-29a-3p, miR-143-3p, miR-152-3p, miR-186-5p, miR-370-3p, and miR-374b-5p may affect the expression of biomolecules of the insulin signaling pathway. Results: Both chronic and intermittent hyperglycemia affects insulin signaling in visceral pre/adipocytes by upregulation of analyzed PI3K/AKT pathway molecules. Both mRNA and protein expression level is more dependent on stage-specific events than the length of the period of high glucose exposure. What is more, miRs expression changes seem to be involved in PI3K/AKT expression regulation in response to hyperglycemic stimulation. Full article
(This article belongs to the Special Issue Protein Kinases in Metabolic Disorders)
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Review

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54 pages, 17225 KiB  
Review
Diabetic Kinome Inhibitors—A New Opportunity for β-Cells Restoration
by Barbara Pucelik, Agata Barzowska, Janusz M. Dąbrowski and Anna Czarna
Int. J. Mol. Sci. 2021, 22(16), 9083; https://doi.org/10.3390/ijms22169083 - 23 Aug 2021
Cited by 10 | Viewed by 4120
Abstract
Diabetes, and several diseases related to diabetes, including cancer, cardiovascular diseases and neurological disorders, represent one of the major ongoing threats to human life, becoming a true pandemic of the 21st century. Current treatment strategies for diabetes mainly involve promoting β-cell differentiation, and [...] Read more.
Diabetes, and several diseases related to diabetes, including cancer, cardiovascular diseases and neurological disorders, represent one of the major ongoing threats to human life, becoming a true pandemic of the 21st century. Current treatment strategies for diabetes mainly involve promoting β-cell differentiation, and one of the most widely studied targets for β-cell regeneration is DYRK1A kinase, a member of the DYRK family. DYRK1A has been characterized as a key regulator of cell growth, differentiation, and signal transduction in various organisms, while further roles and substrates are the subjects of extensive investigation. The targets of interest in this review are implicated in the regulation of β-cells through DYRK1A inhibition—through driving their transition from highly inefficient and death-prone populations into efficient and sufficient precursors of islet regeneration. Increasing evidence for the role of DYRK1A in diabetes progression and β-cell proliferation expands the potential for pharmaceutical applications of DYRK1A inhibitors. The variety of new compounds and binding modes, determined by crystal structure and in vitro studies, may lead to new strategies for diabetes treatment. This review provides recent insights into the initial self-activation of DYRK1A by tyrosine autophosphorylation. Moreover, the importance of developing novel DYRK1A inhibitors and their implications for the treatment of diabetes are thoroughly discussed. The evolving understanding of DYRK kinase structure and function and emerging high-throughput screening technologies have been described. As a final point of this work, we intend to promote the term “diabetic kinome” as part of scientific terminology to emphasize the role of the synergistic action of multiple kinases in governing the molecular processes that underlie this particular group of diseases. Full article
(This article belongs to the Special Issue Protein Kinases in Metabolic Disorders)
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