Next Article in Journal
Usefulness of Amino Acid Profiling in Ovarian Cancer Screening with Special Emphasis on Their Role in Cancerogenesis
Next Article in Special Issue
Molecular Modeling Study for the Design of Novel Peroxisome Proliferator-Activated Receptor Gamma Agonists Using 3D-QSAR and Molecular Docking
Previous Article in Journal
The Lung Microbiome in Idiopathic Pulmonary Fibrosis: A Promising Approach for Targeted Therapies
Previous Article in Special Issue
Activation of PPARα by Oral Clofibrate Increases Renal Fatty Acid Oxidation in Developing Pigs
Article Menu
Issue 12 (December) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2017, 18(12), 2730;

Lysophospholipid-Related Diseases and PPARγ Signaling Pathway

Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan
Clinical Pharmacology Educational Center, Nihon Pharmaceutical University, Ina-machi, Saitama 362-0806, Japan
Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan
Author to whom correspondence should be addressed.
Received: 18 November 2017 / Revised: 14 December 2017 / Accepted: 15 December 2017 / Published: 16 December 2017
(This article belongs to the Special Issue PPARs in Cellular and Whole Body Energy Metabolism)
Full-Text   |   PDF [448 KB, uploaded 16 December 2017]   |  


The nuclear receptor superfamily includes ligand-inducible transcription factors that play diverse roles in cell metabolism and are associated with pathologies such as cardiovascular diseases. Lysophosphatidic acid (LPA) belongs to a family of lipid mediators. LPA and its naturally occurring analogues interact with G protein-coupled receptors on the cell surface and an intracellular nuclear hormone receptor. In addition, several enzymes that utilize LPA as a substrate or generate it as a product are under its regulatory control. Recent studies have demonstrated that the endogenously produced peroxisome proliferator-activated receptor gamma (PPARγ) antagonist cyclic phosphatidic acid (cPA), which is structurally similar to LPA, inhibits cancer cell invasion and metastasis in vitro and in vivo. We recently observed that cPA negatively regulates PPARγ function by stabilizing the binding of the co-repressor protein, a silencing mediator of retinoic acid, and the thyroid hormone receptor. We also showed that cPA prevents neointima formation, adipocyte differentiation, lipid accumulation, and upregulation of PPARγ target gene transcription. The present review discusses the arbitrary aspects of the physiological and pathophysiological actions of lysophospholipids in vascular and nervous system biology. View Full-Text
Keywords: lysophospholipids; PPARγ; vascular diseases; dementia; spinal cord injury lysophospholipids; PPARγ; vascular diseases; dementia; spinal cord injury

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Tsukahara, T.; Matsuda, Y.; Haniu, H. Lysophospholipid-Related Diseases and PPARγ Signaling Pathway. Int. J. Mol. Sci. 2017, 18, 2730.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top