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Biomedicines
Special Issues
PPARs in Health and Disease, 2nd Edition
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PPARs in Health and Disease, 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 1604

Special Issue Editor

Prof. Dr. Maria Konstandi

E-Mail Website
Guest Editor
Department of Pharmacology, Faculty of Medicine, University of Ioannina, Ioannina 45110, Greece
Interests: drug metabolism; PPARα; stress systems biology; neural plasticity; antipsychotics in cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Peroxisome proliferator-activated receptors (PPARs) belong to a nuclear receptor superfamily, acting as ligand-activated transcription factors that exert specific pleiotropic responses. The three known isoforms, PPARα, PPARβ/δ, and PPARγ, have, among other things, determinant roles in energy homeostasis, regulating glucose and lipid metabolism. Upon binding with hormones, lipids, or other ligands, PPARs act by forming heterodimers with retinoic X receptors and, in cooperation with co-repressors or co-activators, regulate several target genes. They are involved in the pathophysiology of metabolic disorders and are pharmaceutical targets for their treatment. Specifically, PPARα and PPARγ agonists are used in the treatment of hyperlipidemia and type 2 diabetes, respectively. It also appears that the activation of PPARs affects carcinogenesis because it can be involved in the complex regulation of cancer cell type-specific proliferation, differentiation, and survival. In the last decade, intensive research has focused on the potential role of PPARα, PPARγ, and PPARβ/δ specific agonists in improving brain cell metabolism and cognitive function in neurodegenerative and neurodevelopmental disorders. PPARs also regulate morphogenesis and the inflammatory response. This Special Issue of Biomedicines includes the most recent advances in the regulation and function of PPARs and provides well-grounded views on therapeutic perspectives for the use of PPAR agonists or antagonists in various disease states, including dyslipidemia, atherosclerosis, obesity, diabetes, neurodegenerative disorders, and cancer.

Prof. Dr. Maria Konstandi
Guest Editor

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Keywords

  • PPARα
  • PPARβ/δ
  • PPARγ
  • nuclear receptor
  • lipid homeostasis
  • glucose homeostasis
  • neurodegenerative disorders
  • dyslipidemia
  • atherosclerosis
  • cardiovascular disease
  • cancer

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Published Papers (1 paper)

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Review

26 pages, 2450 KiB  
Review
Application of PPAR Ligands and Nanoparticle Technology in Metabolic Steatohepatitis Treatment
by Hung Thai Vu, Vien Duc Nguyen, Hiroko Ikenaga and Tsutomu Matsubara
Biomedicines 2024, 12(8), 1876; https://doi.org/10.3390/biomedicines12081876 - 16 Aug 2024
Viewed by 1338
Abstract
Metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH) is a major disease worldwide whose effective treatment is challenging. Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily and function as ligand-activated transcription factors. To date, three distinct subtypes of PPARs have been characterized: PPARα, [...] Read more.
Metabolic dysfunction-associated steatotic liver disease/steatohepatitis (MASLD/MASH) is a major disease worldwide whose effective treatment is challenging. Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily and function as ligand-activated transcription factors. To date, three distinct subtypes of PPARs have been characterized: PPARα, PPARβ/δ, and PPARγ. PPARα and PPARγ are crucial regulators of lipid metabolism that modulate the transcription of genes involved in fatty acid (FA), bile acid, and cholesterol metabolism. Many PPAR agonists, including natural (FAs, eicosanoids, and phospholipids) and synthetic (fibrate, thiazolidinedione, glitazar, and elafibranor) agonists, have been developed. Furthermore, recent advancements in nanoparticles (NPs) have led to the development of new strategies for MASLD/MASH therapy. This review discusses the applications of specific cell-targeted NPs and highlights the potential of PPARα- and PPARγ-targeted NP drug delivery systems for MASLD/MASH treatment. Full article
(This article belongs to the Special Issue PPARs in Health and Disease, 2nd Edition)
►▼ Show Figures

Figure 1

Figure 1
<p>PPAR targets and contributing factors in MASLD/MASH. C1Q and collagen domain containing adiponectin (ADIPOQ) is a key insulin regulator whose secretion from the adipose tissue into the liver is regulated by PPARγ. Insulin regulates SREBP-1C via the PI3K/AKT signaling pathway in the liver. PPARα regulates the essential glycolytic enzymes ACC and FAS that play key roles in the synthesis of TGs. ChREBP is also involved in TG synthesis. LPL and APOC3 promote TG hydrolyzation into FAs. CPT1/2, SLC27A1, ACAD, HMGCS2, and EHHADH are involved in mitochondrial β-oxidation. In the presence of ACC, acetyl-CoA is converted to malonyl-CoA (de novo lipogenesis). Peroxisomal β-oxidation is enhanced via ACOX and DGAT1/2. Excess TG is transported to adipose tissue by VLDL facilitated by the expression of apolipoproteins, APOE and APOC2, and MTTP. In adipose tissues, FAs are converted into TGs via FABP4, CD36, LPL, MOGAT1, and FSP27. FA accumulation can cause autophagy controlled by ATA and TFEB. In MASH, downregulation of TGF-β, TNF-α, and MCP1 levels triggers hepatic inflammation, which subsequently activates the hepatic stellate cells and can lead to fibrosis.</p> Full article ">Figure 2
<p>Single-nuclei RNA sequencing of PPARα and -γ expression levels in human hepatic cells. (<b>A</b>) Uniform manifold approximation and projection (UMAP) plots show the annotations for different cell types. (<b>B</b>) Violin plots of PPARα and PPARγ expression levels with marker genes for nine distinct cell types. (<b>C</b>) Feature plots. <b>Abbreviations:</b> BANK1, B cell scaffold protein with ankyrin repeats 1; KLRF1, killer cell lectin receptor F1; DCN, decorin; KRT7, keratin 7; STAB2, stabilin 2; TAT, tyrosine aminotransferase; CYP3A4, cytochrome P450 family 3 A member 4. <b>Methods:</b> Gene expression patterns of hepatic cells were investigated via single-nucleus RNA-sequencing in healthy individuals and patients with MASLD. Data were obtained from the Gene Expression Omnibus (GEO; accession number GSE174748). The Seurat package (version 5.0.1) was used to analyze the single-cell RNA sequencing data [<a href="#B63-biomedicines-12-01876" class="html-bibr">63</a>]. Filtering was used to remove the cells with ovecellsochondrial genes or fewer than 200 genes. Cells were normalized and clustered using Seurat. The samples were integrated using a harmony approach [<a href="#B64-biomedicines-12-01876" class="html-bibr">64</a>]. Cell types were annotated based on the expression levels of specific gene markers. UMAP, features, and violin plots were generated using the R statistical software (version 4.3.2).</p> Full article ">Figure 3
<p>Schematic diagram of the main types of NPs.</p> Full article ">Figure 4
<p>Passive targeting nanoparticles mechanism.</p> Full article ">
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