Reprint

PPARs as Key Mediators of Metabolic and Inflammatory Regulation

Edited by
May 2022
456 pages
  • ISBN978-3-0365-4192-1 (Hardback)
  • ISBN978-3-0365-4191-4 (PDF)

This book is a reprint of the Special Issue PPARs as Key Mediators of Metabolic and Inflammatory Regulation that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

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 clinics (glitazones and fibrates). The study of PPAR action, also modulated by post-translational 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 includes a broad range of basic and translational article, both original research and reviews, focused on the latest developments in the regulation of metabolic and/or inflammatory processes by PPARs in all organs and the microbiomes of different vertebrate species.

Format
  • Hardback
License
© 2022 by the authors; CC BY-NC-ND license
Keywords
nuclear receptor; gene transcription; inflammation; molecular docking; PPARβ/δ; inflammation; lung; pulmonary artery; GW0742; GSK3787; docking; lipopolysaccharide (LPS); PPARγ ligand; coumarin; fluorescent ligand; screening; crystal structure; PPAR; atopic dermatitis; psoriasis; metabolic reprograming; glucose; fatty acids; mycobacteria; M. tuberculosis; M. leprae; PPARs; lipid droplets; metabolic alterations; hepatic damage; nuclear factors; pharmacological targets; PPARβ/δ; AMPK; GDF15; insulin resistance; type 2 diabetes mellitus; psoriasis; peroxisome proliferator-activated receptor gamma (PPARγ); real-time PCR; ELISA; immunohistochemistry; signaling pathway; PPAR gamma; brain; neural stem cells; infection; neuroinflammation; HIV; Zika; cytomegalovirus; neurogenesis; microglia; inflammation; liver damage; toll-like receptor 4; P2Y2 receptor; metabolic syndrome; resveratrol; quercetin; PPARα; peroxisome; β-oxidation; PPRE; ligand; coregulator; micronutrients; PPARα knockout; adipose tissue; PPAR; browning; lipid metabolism; depression; PPARg; inflammation; neuropathology; corticotropin releasing hormone; norepinephrine; subgenual prefrontal cortex; amygdala; nucleus accumbens; common carotid artery occlusion; electroretinography; fibroblast growth factor 21; pemafibrate; peroxisome proliferator-activated receptor alpha; retinal ischemia; skeletal muscle; inflammation; PPARs; substrate metabolism; nonalcoholic fatty liver disease (NAFLD); sex dimorphism; lipidomics; hepatic sex-biased gene expression; PPARγ; pulmonary arterial hypertension; TGFβ; vascular injury; inflammation; proliferation; kidney fibrosis; pattern-recognition receptors; phagocytosis; nitric oxide synthase; fenofibrate; oleoylethanolamide; palmitoylethanolamide; PPARs; cancer; immunity; obesity; diabetes; miRNA; DNA methylation; histone modification; peroxisome-proliferator-activated receptor; fatty acid oxidation; doping control; regulatory T cells; inflammation; exercise; nuclear receptors; PPARs; nutrigenomics; energy homeostasis; dairy animals; non-alcoholic fatty liver disease (NAFLD); non-alcoholic steatohepatitis (NASH); type 2 diabetes mellitus; peroxisome proliferator-activated receptors (PPAR); bezafibrate; fenofibric acid; pemafibrate; peroxisome proliferator-activated receptor; dual/pan agonist; X-ray crystallography; n/a