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PPAR Update: Molecular Mechanisms and Therapeutic Perspectives
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PPAR Update: Molecular Mechanisms and Therapeutic Perspectives

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 1569

Special Issue Editor

Prof. Dr. Naoki Tanaka

E-Mail Website
Guest Editor
Department of Global Medical Research Promotion, Shinshu University Graduate School of Medicine, Asahi 3-1-1, Matsumoto 390-8621, Japan
Interests: metabolic dysfunction-associated steatotic liver disease (MASLD); metabolic dysfunction-associated steatohepatitis (MASH); nutrient metabolism; PPAR; nutritional intervention; hepatic fibrosis; hepatocarcinogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, “PPAR Update: Molecular Mechanisms and Therapeutic Perspectives”, aims to highlight recent advances in the biology, pharmacology, and translational research of peroxisome proliferator-activated receptor (PPAR). PPARs are key nuclear receptors involved in lipid metabolism, inflammation, and organ protection across the liver, heart, kidney, and other systems. With the emergence of selective PPARα modulators (SPPARMα), such as pemafibrate, novel insights have been gained into ligand selectivity, tissue-specific regulation, and therapeutic applications.

This Special Issue welcomes original research articles and reviews that explore molecular mechanisms, omics-based profiling, structural and computational studies, inter-organ crosstalk, and clinical implications of PPAR signaling. By integrating findings from basic to clinical sciences, this collection aims to provide an updated and comprehensive overview of the evolving field of PPAR biology and its potential for precision medicine.

Prof. Dr. Naoki Tanaka
Guest Editor

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • PPAR
  • PPARα
  • SPPARMα
  • pemafibrate
  • lipid metabolism
  • inflammation
  • fibrosis
  • nuclear receptor
  • translational research
  • precision medicine

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Published Papers (2 papers)

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Research

18 pages, 7868 KB  
Article
Hepatocyte PPARα Is Essential for Triglyceride-Lowering Effect of Pemafibrate
by Zhe Zhang, Xuguang Zhang, Chufang Qian, Pan Diao, Takero Nakajima, Takefumi Kimura, Frank J. Gonzalez and Naoki Tanaka
Int. J. Mol. Sci. 2026, 27(7), 3308; https://doi.org/10.3390/ijms27073308 - 6 Apr 2026
Viewed by 340
Abstract
We previously demonstrated that a clinically relevant dose of pemafibrate (PEM), a selective peroxisome proliferator-activated receptor α (PPARα) modulator (SPPARMα), reduces serum triglyceride (TG) levels in mice via hepatic PPARα activation. However, the specific contribution of hepatocyte PPARα remains unclear. To address this, [...] Read more.
We previously demonstrated that a clinically relevant dose of pemafibrate (PEM), a selective peroxisome proliferator-activated receptor α (PPARα) modulator (SPPARMα), reduces serum triglyceride (TG) levels in mice via hepatic PPARα activation. However, the specific contribution of hepatocyte PPARα remains unclear. To address this, male Ppara-floxed (Pparafl/fl) and hepatocyte-specific Ppara-disrupted (PparaΔHep) mice were fed a diet with or without a clinically relevant dose of PEM (0.00005%) for four weeks. In Pparafl/fl mice, PEM significantly reduced circulating TG and non-esterified fatty acid levels by enhancing hepatic fatty acid uptake and β-oxidation. In contrast, these effects were absent in PparaΔHep mice. Notably, PEM did not activate PPARα in extrahepatic tissues, including white/brown adipose tissue, kidney, and skeletal muscle in either genotype. These findings underscore the essential role of hepatocyte PPARα in mediating the pharmacological effects of PEM at clinically relevant doses. Full article
(This article belongs to the Special Issue PPAR Update: Molecular Mechanisms and Therapeutic Perspectives)
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11 pages, 1581 KB  
Article
Peroxisome Proliferator-Activated Receptor α/δ/γ Activation Profile by Endogenous Long-Chain Fatty Acids
by Akihiro Honda, Aoi Hosoda, Waka Kamichatani, Midori Ogasawara, Shiori Miyazaki, Nonoka Kashiwagi, Shotaro Kamata and Isao Ishii
Int. J. Mol. Sci. 2025, 26(24), 12020; https://doi.org/10.3390/ijms262412020 - 13 Dec 2025
Cited by 1 | Viewed by 889
Abstract
There is a wealth of information available about endogenous fatty acid ligands for peroxisome proliferator-activated receptor α/δ/γ (PPARα/δ/γ); however, there are few comparative studies of PPARα/δ/γ activation using standardized experimental systems. This study investigated which of 14 major free long-chain fatty acids (LCFAs: [...] Read more.
There is a wealth of information available about endogenous fatty acid ligands for peroxisome proliferator-activated receptor α/δ/γ (PPARα/δ/γ); however, there are few comparative studies of PPARα/δ/γ activation using standardized experimental systems. This study investigated which of 14 major free long-chain fatty acids (LCFAs: C12:0–C22:6) and 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) activate PPARα/δ/γ using a coactivator recruitment assay. We recently discovered that eight different synthetic PPAR agonists recruit four different coactivator peptides (PGC1α, CBP, SRC1, TRAP220) with varying potency and efficacy, so we examined the ligand-concentration-dependent recruitment of these four coactivators. All 15 fatty acids (FAs) activated PPARα/δ at high concentrations, but only palmitic acid, stearic acid, oleic acid, and linoleic acid significantly activated PPARα/δ at physiologically relevant concentrations. Lauric acid, myristic acid, palmitic acid, and 15d-PGJ2 activated PPARγ at high concentrations, but only palmitic acid slightly activated PPARγ at physiologically relevant concentrations. FA ligands exhibited different coactivator preference compared to synthetic PPAR agonists, including approved drugs such as pemafibrate, seladelpar, and pioglitazone, suggesting that these agonists may regulate target gene transcription in a different manner than natural FA ligands. Such differences may be relevant to the pathogenesis of side effects of synthetic PPAR agonists occasionally observed in (pre)clinical studies. Full article
(This article belongs to the Special Issue PPAR Update: Molecular Mechanisms and Therapeutic Perspectives)
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