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Special Issue "Role of PPAR Receptors in Human Health and Disease"

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 30 November 2019

Special Issue Editors

Guest Editor
Prof. Dr. Raffaele Capasso

Universita degli Studi di Napoli Federico II, Naples, Italy
Website | E-Mail
Interests: role of cannabinoid, vanilloid and kappa-opioid receptors in the gastrointestinal tract; ethnopharmacological studies on medicinal plants; clinical pharmacology of herbal products; nutritional pharmacology
Guest Editor
Dr. Fabio Arturo Iannotti

Endocannabinoid Research Group, Consiglio Nazionale delle Ricerche, Rome, Italy
Website | E-Mail
Interests: PPARs; Muscular Degenerative Diseases; Endocannabinoid System; Epilepsy; Ion Channels

Special Issue Information

Dear Colleagues,

The research on cannabinoids and congeners is currently growing. Among the different classes of receptors related to the activity of these molecules, a great attention has been focused on the role of peroxisome proliferator-activated receptors (PPARs). The family of PPARs encompasses three distinct members named PPARα, PPARβ/δ, and PPARγ. PPARα activity is mainly implicated in the metabolism of lipids, carbohydrates, and amino acids; PPARγ is mostly involved in the regulation of adipogenesis, energy balance, and lipid biosynthesis; PPARβ/δ regulates fatty acid oxidation in skeletal and cardiac muscles. There is compelling evidence demonstrating that both natural and synthetic ligands, such as fatty acids, eicosanoids, phytanic acid, fibrates, palmitoylethanolamide, etc., can be used to regulate the expression and function of PPARs for the treatment of various human disorders. Therefore, the understanding of the molecular mechanisms and role of PPARs in nutrition and therapeutic treatment is the focus of this Special Issue.

Prof. Dr. Raffaele Capasso
Dr. Fabio Arturo Iannotti
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. Molecules is an international peer-reviewed open access semimonthly 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 1800 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

  • PPAR receptors
  • Natural and synthetic molecules
  • Intracellular cascades
  • PPARs and nutrition
  • PPARs and health

Published Papers (2 papers)

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Research

Open AccessArticle
Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model
Molecules 2019, 24(2), 270; https://doi.org/10.3390/molecules24020270
Received: 1 December 2018 / Revised: 4 January 2019 / Accepted: 8 January 2019 / Published: 12 January 2019
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Abstract
Myocardial infarction (MI) initiates an inflammatory response that promotes both beneficial and deleterious effects. The early response helps the myocardium to remove damaged tissue; however, a prolonged later response brings cardiac remodeling characterized by functional, metabolic, and structural pathological changes. Current pharmacological treatments [...] Read more.
Myocardial infarction (MI) initiates an inflammatory response that promotes both beneficial and deleterious effects. The early response helps the myocardium to remove damaged tissue; however, a prolonged later response brings cardiac remodeling characterized by functional, metabolic, and structural pathological changes. Current pharmacological treatments have failed to reverse ischemic-induced cardiac damage. Therefore, our aim was to study if clofibrate treatment was capable of decreasing inflammation and apoptosis, and reverse ventricular remodeling and MI-induced functional damage. Male Wistar rats were assigned to (1) Sham coronary artery ligation (Sham) or (2) Coronary artery ligation (MI). Seven days post-MI, animals were further divided to receive vehicle (V) or clofibrate (100 mg/kg, C) for 7 days. The expression of IL-6, TNF-α, and inflammatory related molecules ICAM-1, VCAM-1, MMP-2 and -9, nuclear NF-kB, and iNOS, were elevated in MI-V. These inflammatory biomarkers decreased in MI-C. Also, apoptotic proteins (Bax and pBad) were elevated in MI-V, while clofibrate augmented anti-apoptotic proteins (Bcl-2 and 14-3-3ε). Clofibrate also protected MI-induced changes in ultra-structure. The ex vivo evaluation of myocardial functioning showed that left ventricular pressure and mechanical work decreased in infarcted rats; clofibrate treatment raised those parameters to control values. Echocardiogram showed that clofibrate partially reduced LV dilation. In conclusion, clofibrate decreases cardiac remodeling, decreases inflammatory molecules, and partly preserves myocardial diameters. Full article
(This article belongs to the Special Issue Role of PPAR Receptors in Human Health and Disease)
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Open AccessArticle
PPARα Agonist Suppresses Inflammation after Corneal Alkali Burn by Suppressing Proinflammatory Cytokines, MCP-1, and Nuclear Translocation of NF-κB
Molecules 2019, 24(1), 114; https://doi.org/10.3390/molecules24010114
Received: 28 November 2018 / Revised: 24 December 2018 / Accepted: 24 December 2018 / Published: 29 December 2018
PDF Full-text (5455 KB) | HTML Full-text | XML Full-text
Abstract
We investigated the effect of a peroxisome proliferator-activated receptor α (PPARα) agonist after corneal alkali injury. Fenofibrate 0.05% (PPARα agonist group) or vehicle (Vehicle group) was topically instilled onto the rat cornea after injury. Histological, immunohistochemical, and real-time reverse transcription PCR analyses were [...] Read more.
We investigated the effect of a peroxisome proliferator-activated receptor α (PPARα) agonist after corneal alkali injury. Fenofibrate 0.05% (PPARα agonist group) or vehicle (Vehicle group) was topically instilled onto the rat cornea after injury. Histological, immunohistochemical, and real-time reverse transcription PCR analyses were performed. PPARα-positive cells were observed among basal cells of the corneal epithelium in normal and alkali-burned corneas. The number of infiltrating neutrophils and macrophages at the corneal limbus was lower in the PPARα agonist group. Interleukin-1β (IL-1β), IL-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and vascular endothelial growth factor-An mRNA expression was suppressed in the PPARα agonist group compared to the Vehicle group. mRNA levels of nuclear factor kappa B (NF-κB) in corneal tissue were not different. However, NF-κB was expressed in the cytoplasm of basal cells in the PPARα agonist group and in the nucleus in the Vehicle group. MCP-1 was more weakly expressed in the PPARα agonist group. The PPARα agonist inhibited inflammation during the early phase after injury. Anti-inflammatory effects of the PPARα agonist included prevention of up-regulation of proinflammatory cytokines and MCP-1, and prevention of inflammatory cell infiltration into the injured cornea. Thus, a PPARα agonist may be a promising treatment for corneal injury. Full article
(This article belongs to the Special Issue Role of PPAR Receptors in Human Health and Disease)
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