Redox Regulation in Immunometabolism

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 October 2023) | Viewed by 1554

Special Issue Editors


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Guest Editor
Department of Genetics, Evolution, Microbiology and Immunology, University of Campinas, Campinas 13083-862, SP, Brazil
Interests: AhR modulation; macrophage activation/ metabolism; obesity; immunology

E-Mail Website
Guest Editor
Department of Genetics, Evolution, Microbiology and Immunology, University of Campinas, Campinas 13083-862, SP, Brazil
Interests: genetics; immunometabolism; cancer

E-Mail Website
Guest Editor
Department of Genetics, Microbiology and Immunology, University of Campinas (UNICAMP), Campinas 13083-862, Brazil
Interests: immunometabolism; inflammatory response; inflammation; obesity; type 2 diabetes

Special Issue Information

Dear colleagues,

Over the last decades, several works have shown how the metabolic regulation of immune cells impacts their activation and effector function, consolidating a field called “immunometabolism”. These metabolic modulations control the bioenergetic and biosynthetic processes of immune cells and regulate their responses during infections and autoimmune diseases. Oxidation–reduction (redox) reactions are indispensable for properly regulating biochemical reactions that maintain cell metabolism, making them essential for the maintenance of life. Different immune cells that perform specific functions utilize a distinct number of metabolic pathways to generate the energy levels necessary to perform their activities and produce biosynthetic intermediates that allow them to function properly. Moreover, the redox reactions associated with electron transference among the metabolic pathways can produce oxidative molecules that contribute to the effector function of immune cells, but also may cause tissue damage through an uncontrolled inflammatory response. This Special Issue aims to report on the latest knowledge about the relationship between redox regulation and metabolic and functional control of immune cells, focusing on the role of the redox balance in homeostasis and diseases.

Dr. Bianca Gazieri Castelucci
Dr. Larissa Menezes dos Reis
Dr. Pedro Manoel Mendes Moraes-Vieira
Guest Editors

Manuscript Submission Information

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Keywords

  • inflammation
  • metabolism
  • mitochondria
  • redox
  • immune cells
  • glycolysis
  • reactive oxygen species
  • adipokines
  • immunometabolism
  • metabolites

Published Papers (1 paper)

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Research

23 pages, 3752 KiB  
Article
Highly Selective MIF Ketonase Inhibitor KRP-6 Diminishes M1 Macrophage Polarization and Metabolic Reprogramming
by Eszter Vámos, Nikoletta Kálmán, Eva Maria Sturm, Barsha Baisakhi Nayak, Julia Teppan, Viola Bagóné Vántus, Dominika Kovács, Lilla Makszin, Tamás Loránd, Ferenc Gallyas, Jr. and Balázs Radnai
Antioxidants 2023, 12(10), 1790; https://doi.org/10.3390/antiox12101790 - 22 Sep 2023
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Abstract
Macrophage polarization is highly involved in autoimmunity. M1 polarized macrophages drive inflammation and undergo metabolic reprogramming, involving downregulation of mitochondrial energy production and acceleration of glycolysis. Macrophage migration inhibitory factor (MIF), an enigmatic tautomerase (ketonase and enolase), was discovered to regulate M1 polarization. [...] Read more.
Macrophage polarization is highly involved in autoimmunity. M1 polarized macrophages drive inflammation and undergo metabolic reprogramming, involving downregulation of mitochondrial energy production and acceleration of glycolysis. Macrophage migration inhibitory factor (MIF), an enigmatic tautomerase (ketonase and enolase), was discovered to regulate M1 polarization. Here, we reveal that KRP-6, a potent and highly selective MIF ketonase inhibitor, reduces MIF-induced human blood eosinophil and neutrophil migration similarly to ISO-1, the most investigated tautomerase inhibitor. We equally discovered that KRP-6 prevents M1 macrophage polarization and reduces ROS production in IFN-γ-treated cells. During metabolic reprogramming, KRP-6 improved mitochondrial bioenergetics by ameliorating basal respiration, ATP production, coupling efficiency and maximal respiration in LPS+IFN-γ-treated cells. KRP-6 also reduced glycolytic flux in M1 macrophages. Moreover, the selective MIF ketonase inhibitor attenuated LPS+IFN-γ-induced downregulation of PARP-1 and PARP-2 mRNA expression. We conclude that KRP-6 represents a promising novel therapeutic compound for autoimmune diseases, which strongly involves M1 macrophage polarization. Full article
(This article belongs to the Special Issue Redox Regulation in Immunometabolism)
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