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Recent Advances in the Interaction between Metabolism and Inflammation
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Recent Advances in the Interaction between Metabolism and Inflammation

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 October 2020) | Viewed by 5718

Special Issue Editor

Dr. Jong-Seok Moon

E-Mail Website
Guest Editor
Department of Integrated Biomedical Science, Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University, Cheonan-si, Korea
Interests: inflammasome; necrosome; immunometabolism; metabolic cell death; human metabolic diseases

Special Issue Information

Dear Colleagues,

Metabolism and inflammation are linked to the pathogenesis of human chronic diseases including type 2 diabetes, atherosclerosis and Alzheimer’s diseases. Alteration of metabolic pathways could regulate inflammatory responses in immune cells. On the other hand, elevated inflammatory cytokines could lead to changes in various metabolic pathways in secondary cells such as epithelial cells, fibroblasts, adipocytes and neuronal cells. The understanding of the connection between metabolism and inflammation is important for the discovery of new mechanisms or therapeutic approaches to cure human chronic metabolic diseases.

Therefore, we need to investigate the mechanism by which the metabolism–inflammation axis, which is regulated by various genes in cells or tissues, operates. This includes the role of the metabolic pathway or intra-cellular metabolites in the activation of pro-inflammatory or anti-inflammatory responses in immune cells; the roles of metabolites, which come from outside cells, in the regulation of such responses; and the roles of pro- or anti-inflammatory cytokines in the regulation of the cellular metabolic pathway in secondary cells.

This Special Issue aims to present new knowledge on the interaction between metabolism and inflammation to inform the future research direction on the discovery of genes that play critical roles in human diseases. To this end, we invite papers reporting novel findings related to the special topics which are The mechanism by which cellular metabolic pathway regulates inflammation in immune cells and the mechanism by which cytokine-dependent signaling pathway  regulates cellular metabolism in cells.

Dr. Jong-Seok Moon
Guest Editor

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. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • Metabolism
  • Inflammation
  • Metabolic diseases
  • Metabolites
  • Cytokines

Published Papers (2 papers)

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Research

14 pages, 17515 KiB  
Article
Allergic Inflammation Alters microRNA Expression Profile in Adipose Tissue in the Rat
by Dawid Szczepankiewicz, Wojciech Langwiński, Paweł Kołodziejski, Ewa Pruszyńska-Oszmałek, Maciej Sassek, Joanna Nowakowska, Agata Chmurzyńska, Krzysztof W. Nowak and Aleksandra Szczepankiewicz
Genes 2020, 11(9), 1034; https://doi.org/10.3390/genes11091034 - 2 Sep 2020
Cited by 3 | Viewed by 2496
Abstract
Adipose tissue is a major source of circulating exosomal microRNAs (miRNAs) that are modulators of the immune response in various types of tissues and organs, including airways. Still, no evidence exists if allergic airway inflammation may affect fat tissue inflammation via alterations in [...] Read more.
Adipose tissue is a major source of circulating exosomal microRNAs (miRNAs) that are modulators of the immune response in various types of tissues and organs, including airways. Still, no evidence exists if allergic airway inflammation may affect fat tissue inflammation via alterations in the miRNA expression profile. Therefore, we investigated the miRNA expression profile in the adipose tissue upon induced allergic inflammation in the airways in the rat. Brown Norway rats were chronically sensitized to house dust mite extract for seven weeks. Body composition was performed using MiniSpec Plus. The eosinophil count and the total IgE level were determined to confirm the induction of allergic inflammation. MiRNA expression profiling was done using the next-generation sequencing with validation by qPCR. We found that allergic airway inflammation significantly increased fat in adipose tissue, glucose concentration, and the gene expression of adipose tissue-derived proinflammatory peptides (leptin, TNFα). In miRNA-seq analysis, we showed significant differences in the expression of 36 mature miRNAs, three precursors, and two miRNA families in adipose tissue of allergic rats. Two miRNAs—miRNA-151-5p and miRNA-423-3p—showed significantly increased expression in qPCR in adipose tissue and lungs of sensitized animals. Allergic airway inflammation affects fat tissue and alters miRNA expression profile in adipose tissue in the rat. Full article
(This article belongs to the Special Issue Recent Advances in the Interaction between Metabolism and Inflammation)
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13 pages, 1871 KiB  
Article
NOX4 Deficiency Exacerbates the Impairment of Cystatin C-Dependent Hippocampal Neurogenesis by a Chronic High Fat Diet
by Piyanart Jiranugrom, Ik Dong Yoo, Min Woo Park, Ji Hwan Ryu, Jong-Seok Moon and Sun Shin Yi
Genes 2020, 11(5), 567; https://doi.org/10.3390/genes11050567 - 19 May 2020
Cited by 4 | Viewed by 2944
Abstract
Hippocampal neurogenesis is linked with a cognitive process under a normal physiological condition including learning, memory, pattern separation, and cognitive flexibility. Hippocampal neurogenesis is altered by multiple factors such as the systemic metabolic changes. NADPH oxidase 4 (NOX4) has been implicated in the [...] Read more.
Hippocampal neurogenesis is linked with a cognitive process under a normal physiological condition including learning, memory, pattern separation, and cognitive flexibility. Hippocampal neurogenesis is altered by multiple factors such as the systemic metabolic changes. NADPH oxidase 4 (NOX4) has been implicated in the regulation of brain function. While the role of NOX4 plays in the brain, the mechanism by which NOX4 regulates hippocampal neurogenesis under metabolic stress is unclear. In this case, we show that NOX4 deficiency exacerbates the impairment of hippocampal neurogenesis by inhibiting neuronal maturation by a chronic high fat diet (HFD). NOX4 deficiency resulted in less hippocampal neurogenesis by decreasing doublecortin (DCX)-positive neuroblasts, a neuronal differentiation marker, and their branched-dendrites. Notably, NOX4 deficiency exacerbates the impairment of hippocampal neurogenesis by chronic HFD. Moreover, NOX4 deficiency had a significant reduction of Cystatin C levels, which is critical for hippocampal neurogenesis, under chronic HFD as well as normal chow (NC) diet. Furthermore, the reduction of Cystatin C levels was correlated with the impairment of hippocampal neurogenesis in NOX4 deficient and wild-type (WT) mice under chronic HFD. Our results suggest that NOX4 regulates the impairment of Cystatin C-dependent hippocampal neurogenesis under chronic HFD. Full article
(This article belongs to the Special Issue Recent Advances in the Interaction between Metabolism and Inflammation)
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