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: closed (30 April 2025) | Viewed by 1953

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Department of Pharmacology, Faculty of Medicine, University of Ioannina, Ioannina 45110, Greece
Interests: drug metabolism; PPARα; stress systems biology; neural plasticity; antipsychotics in cancer
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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 (2 papers)

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Research

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19 pages, 8196 KiB  
Article
Dual Modulation of Adipogenesis and Apoptosis by PPARG Agonist Rosiglitazone and Antagonist Betulinic Acid in 3T3-L1 Cells
by Patsawee Sriboonaied, Pornwipa Phuangbubpha, Puretat Saetan, Purin Charoensuksai and Adisri Charoenpanich
Biomedicines 2025, 13(6), 1340; https://doi.org/10.3390/biomedicines13061340 (registering DOI) - 30 May 2025
Abstract
Background/Objectives: Disruptions in adipose tissue dynamics contribute to obesity-related metabolic disorders, emphasizing the need for targeted therapies focusing on adipose tissue cells, including progenitor cells and adipocytes. Peroxisome proliferator-activated receptor gamma (PPARG) ligands are potent insulin sensitizers used in type 2 diabetes treatment. [...] Read more.
Background/Objectives: Disruptions in adipose tissue dynamics contribute to obesity-related metabolic disorders, emphasizing the need for targeted therapies focusing on adipose tissue cells, including progenitor cells and adipocytes. Peroxisome proliferator-activated receptor gamma (PPARG) ligands are potent insulin sensitizers used in type 2 diabetes treatment. This study investigated the effects of rosiglitazone, a PPARG agonist, and betulinic acid, a PPARG antagonist, on adipogenesis and apoptosis in 3T3-L1 pre-adipocytes. Method: 3T3-L1 pre-adipocytes were treated with rosiglitazone or betulinic acid during adipogenic differentiation. Lipid droplet formation was used to evaluate adipogenesis. Cell growth and cell death were assessed using the resazurin-based cell viability assay, trypan blue exclusion assay, LDH assay, and Annexin V/PI staining. Quantitative PCR was conducted to examine the expression of genes associated with adipogenesis and apoptosis. Results: Betulinic acid reduced adipogenesis only when administered daily for eight days. Rosiglitazone did not alter the overall lipid quantity; however, it promoted a shift toward fewer but larger lipid droplets. Both compounds increased Adipoq and Cfd expression, and betulinic acid also elevated Fabp4. Rosiglitazone induced stronger cell aggregation. Despite increased cell death, overall viability was maintained. Apoptotic cell death was enhanced by both compounds and confirmed via Annexin V/PI staining and flow cytometry, accompanied by downregulation of Ccnd1 and Bcl2. Additionally, rosiglitazone markedly increased the expression of Cebpa, a key regulator that can modulate lipid droplet formation and the balance between cell growth and death. Conclusions: Rosiglitazone and betulinic acid differentially modulate adipogenesis and apoptosis in 3T3-L1 cells, revealing a complex interplay between lipid accumulation and programmed cell death. Together, the findings underscore the potential of dual PPARG-targeting approaches for metabolic disease interventions. Full article
(This article belongs to the Special Issue PPARs in Health and Disease, 2nd Edition)
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Review

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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
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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)
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