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Inflammation Networks and Chronic Diseases: Molecules and Methods

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 2974

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Guest Editor
Women’s Health and Perinatology Research Group, Department of Clinical Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway
Interests: liposomes; drug delivery; reproductive health; inflammation; chronic diseases; antioxidative activity; oxidative stress biomarkers; functional foods; phytochemicals; natural medicines
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Special Issue Information

Dear Colleagues,

Inflammation is a physiological response with vital consequences in the living system. Acute inflammation is a protective measure against pathogens and essential for cell vitalization. However, chronic inflammation beyond the tolerance of the body system leads to chronic diseases such as cancers, diabetes, hypertension, and Alzheimer´s disease. Inflammation plays the central role in the progression and development of all these chronic diseases with the support of an active role played by a complex network of some vicious molecules such as TNF-a, IL-1b INF-g, and NF-kB and their corresponding receptor molecules, although the symptoms and diseases are completely unrelated.

Although the exact relationships are still unclear, our foods, environments, and living habits have shown direct effects on the progression of such chronic diseases. Understanding the complete networks and functions of inflammation-causing molecule networks may allow us to find cures and treatments for such incurable diseases. Moreover, the identification of the roles played by inflammation network systems in the progression of chronic diseases is very important for developing a modern approach to therapeutic strategies. Therefore, this Special Issue is dedicated to presenting the latest research findings on complete networks and functions of inflammation-causing molecules and methods. I look forward to receiving your contributions to this Special Issue.

Prof. Dr. Purusotam Basnet
Guest Editor

Manuscript Submission Information

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Keywords

  • Inflammation
  • Inflammatory molecules
  • Inflammatory networks
  • Chronic disease
  • Nanomedicines
  • Nanocarriers
  • Smart drug
  • Functional foods

Published Papers (1 paper)

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Research

14 pages, 2307 KiB  
Article
A Michael Acceptor Analogue, SKSI-0412, Down-Regulates Inflammation and Proliferation Factors through Suppressing Signal Transducer and Activator of Transcription 3 Signaling in IL-17A-Induced Human Keratinocyte
by A-Ram Kim, Seungbeom Lee, Jung U Shin, Seung Hui Seok, Young-Ger Suh and Dong Hyun Kim
Int. J. Mol. Sci. 2021, 22(16), 8813; https://doi.org/10.3390/ijms22168813 - 16 Aug 2021
Cited by 1 | Viewed by 2479
Abstract
The activation of signal transducer and activator of transcription 3 (STAT3), as well as up-regulation of cytokines and growth factors to promote STAT3 activation, have been found in the epidermis of psoriatic lesions. Recently, a series of synthetic compounds possessing the Michael acceptor [...] Read more.
The activation of signal transducer and activator of transcription 3 (STAT3), as well as up-regulation of cytokines and growth factors to promote STAT3 activation, have been found in the epidermis of psoriatic lesions. Recently, a series of synthetic compounds possessing the Michael acceptor have been reported as STAT3 inhibitors by covalently binding to cysteine of STAT3. We synthesized a Michael acceptor analog, SKSI-0412, and confirmed the binding affinity between STAT3 and SKSI-0412. We hypothesized that the SKSI-0412 can inhibit interleukin (IL)-17A-induced inflammation in keratinocytes. The introduction of IL-17A increased the phosphorylation of STAT3 in keratinocytes, whereas the inactivation of STAT3 by SKSI-0412 reduced IL-17A-induced STAT3 phosphorylation and IκBζ expression. In addition, human β defensin-2 and S100A7, which are regulated by IκBζ, were significantly decreased with SKSI-0412 administration. We also confirmed that SKSI-0412 regulates cell proliferation, which is the major phenotype of psoriasis. Based on these results, we suggest targeting STAT3 with SKSI-0412 as a novel therapeutic strategy to regulate IL-17A-induced psoriatic inflammation in keratinocytes. Full article
(This article belongs to the Special Issue Inflammation Networks and Chronic Diseases: Molecules and Methods)
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