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Special Issue "PPARs as Key Mediators of Metabolic and Inflammatory Regulation"

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

Deadline for manuscript submissions: 31 July 2021.

Special Issue Editors

Prof. Dr. Manuel Vázquez-Carrera
E-Mail Website
Guest Editor
Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Institute of Biomedicine of the University of Barcelona (IBUB), University of Barcelona, Barcelona, Spain, and Spanish Biomedical Research Center in Diabetes and Associated Metabolic Diseases (CIBERDEM)-Instituto de Salud Carlos III, Madrid, Spain
Interests: insulin resistance; inflammation; type 2 diabetes mellitus; non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH); atherogenic dyslipidemia; diabetic cardiomyopathy; skeletal muscle
Prof. Dr. Walter Wahli
E-Mail Website1 Website2
Guest Editor
Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore 308232, Singapore
Center for Integrative Genomics, University of Lausanne, CH-1015 Lausanne, Switzerland
Interests: nuclear receptor superfamily; gene regulation and gene expression profiling; metabolic regulations; development; skin and wound healing; cancer; liver physiology; non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH); adipose tissue; muscle and exercise; gut; microbiota; inter-organ cross-talk; nutrition; nutrigenetics and nutrigenomics
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Special Issue Information

Dear Colleagues,

Mounting evidence suggests a bidirectional relationship between metabolism and inflammation. Molecular crosstalk between these processes occurs at different levels with the participation of nuclear receptors, including peroxisome proliferator-activated receptors (PPARs). There are three PPAR isotypes α, β/δ, and γ, which modulate metabolic and inflammatory pathways, making them key for the control of cellular, organ, and systemic processes. PPAR activity is governed by fatty acids and fatty acid derivatives, and by drugs used in the clinics (glitazones and fibrates). The study of PPAR action, also modulated by posttranslational modifications, has enabled extraordinary advances in the understanding of the multifaceted roles of these receptors in metabolism, energy homeostasis, and inflammation both in health and disease. This Special Issue of IJMS welcomes a broad range of basic and translational original and review articles focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiome of different vertebrate species.

Prof. Dr. Manuel Vázquez-Carrera
Prof. Dr. Walter Wahli
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 papers will be 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

  • Peroxisome proliferator-activated receptors (PPARs)
  • Organ crosstalk
  • Energy homeostasis
  • Lipids and carbohydrates
  • Metabolic regulations
  • Metabolic diseases
  • Regulation of inflammation
  • Inflammation and immunity
  • Meta-inflammation
  • Inflammatory diseases
  • Metabolic endotoxemia
  • Metabolic reprogramming and inflammation
  • Systems biology
  • Host–microbiota crosstalk

Published Papers (2 papers)

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Research

Open AccessArticle
Synthesis of a Coumarin-Based PPARγ Fluorescence Probe for Competitive Binding Assay
Int. J. Mol. Sci. 2021, 22(8), 4034; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084034 - 14 Apr 2021
Viewed by 286
Abstract
Peroxisome proliferator-activated receptor γ (PPARγ) is a molecular target of metabolic syndrome and inflammatory disease. PPARγ is an important nuclear receptor and numerous PPARγ ligands were developed to date; thus, efficient assay methods are important. Here, we investigated the incorporation of 7-diethylamino coumarin [...] Read more.
Peroxisome proliferator-activated receptor γ (PPARγ) is a molecular target of metabolic syndrome and inflammatory disease. PPARγ is an important nuclear receptor and numerous PPARγ ligands were developed to date; thus, efficient assay methods are important. Here, we investigated the incorporation of 7-diethylamino coumarin into the PPARγ agonist rosiglitazone and used the compound in a binding assay for PPARγ. PPARγ-ligand-incorporated 7-methoxycoumarin, 1, showed weak fluorescence intensity in a previous report. We synthesized PPARγ-ligand-incorporating coumarin, 2, in this report, and it enhanced the fluorescence intensity. The PPARγ ligand 2 maintained the rosiglitazone activity. The obtained partial agonist 6 appeared to act through a novel mechanism. The fluorescence intensity of 2 and 6 increased by binding to the ligand binding domain (LBD) of PPARγ and the affinity of reported PPARγ ligands were evaluated using the probe. Full article
(This article belongs to the Special Issue PPARs as Key Mediators of Metabolic and Inflammatory Regulation)
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Open AccessArticle
Co-Incubation with PPARβ/δ Agonists and Antagonists Modeled Using Computational Chemistry: Effect on LPS Induced Inflammatory Markers in Pulmonary Artery
Int. J. Mol. Sci. 2021, 22(6), 3158; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063158 - 19 Mar 2021
Viewed by 333
Abstract
Peroxisome proliferator activated receptor beta/delta (PPARβ/δ) is a nuclear receptor ubiquitously expressed in cells, whose signaling controls inflammation. There are large discrepancies in understanding the complex role of PPARβ/δ in disease, having both anti- and pro-effects on inflammation. After ligand activation, PPARβ/δ regulates [...] Read more.
Peroxisome proliferator activated receptor beta/delta (PPARβ/δ) is a nuclear receptor ubiquitously expressed in cells, whose signaling controls inflammation. There are large discrepancies in understanding the complex role of PPARβ/δ in disease, having both anti- and pro-effects on inflammation. After ligand activation, PPARβ/δ regulates genes by two different mechanisms; induction and transrepression, the effects of which are difficult to differentiate directly. We studied the PPARβ/δ-regulation of lipopolysaccharide (LPS) induced inflammation (indicated by release of nitrite and IL-6) of rat pulmonary artery, using different combinations of agonists (GW0742 or L−165402) and antagonists (GSK3787 or GSK0660). LPS induced release of NO and IL-6 is not significantly reduced by incubation with PPARβ/δ ligands (either agonist or antagonist), however, co-incubation with an agonist and antagonist significantly reduces LPS-induced nitrite production and Nos2 mRNA expression. In contrast, incubation with LPS and PPARβ/δ agonists leads to a significant increase in Pdk−4 and Angptl−4 mRNA expression, which is significantly decreased in the presence of PPARβ/δ antagonists. Docking using computational chemistry methods indicates that PPARβ/δ agonists form polar bonds with His287, His413 and Tyr437, while antagonists are more promiscuous about which amino acids they bind to, although they are very prone to bind Thr252 and Asn307. Dual binding in the PPARβ/δ binding pocket indicates the ligands retain similar binding energies, which suggests that co-incubation with both agonist and antagonist does not prevent the specific binding of each other to the large PPARβ/δ binding pocket. To our knowledge, this is the first time that the possibility of binding two ligands simultaneously into the PPARβ/δ binding pocket has been explored. Agonist binding followed by antagonist simultaneously switches the PPARβ/δ mode of action from induction to transrepression, which is linked with an increase in Nos2 mRNA expression and nitrite production. Full article
(This article belongs to the Special Issue PPARs as Key Mediators of Metabolic and Inflammatory Regulation)
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