Table of Contents Author Guidelines Submit a Manuscript

A corrigendum for this article has been published. To view the corrigendum, please click here.

PPAR Research
Volume 2016, Article ID 7407153, 8 pages
Clinical Study

Pioglitazone Attenuates Drug-Eluting Stent-Induced Proinflammatory State in Patients by Blocking Ubiquitination of PPAR

1Department of Cardiology, First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, China
2Department of Medicine, Gansu Provincial Hospital of TCM, Lanzhou 730050, China
3Department of Cardiology, Xi’an Central Hospital, Xi’an 710003, China

Received 23 December 2015; Revised 11 April 2016; Accepted 16 May 2016

Academic Editor: Alexander N. Orekhov

Copyright © 2016 Zhongxia Wang et al. 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.


The inflammatory response after polymer-based drug-eluting stent (DES) placement has recently emerged as a major concern. The biologic roles of peroxisome proliferator-activated receptor- (PPAR-) activators thiazolidinedione (TZD) remain controversial in cardiovascular disease. Herein, we investigated the antiinflammatory effects of pioglitazone (PIO) on circulating peripheral blood mononuclear cells (MNCs) in patients after coronary DES implantation. Methods and Results. Twenty-eight patients with coronary artery disease and who underwent DES implantations were randomly assigned to pioglitazone (30 mg/d; PIO) or placebo (control; Con) treatment in addition to optimal standard therapy. After 12 weeks of treatment, plasma concentrations of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor- (TNF-), and matrix metalloproteinase-9 (MMP-9) were significantly decreased in PIO group compared to the Con group (, 0.011, 0.008, and 0.012, resp.). DES-induced mRNA expressions of IL-6, TNF-, and MMP-9 in circulating MNC were significantly blocked by PIO (, 0.012, and 0.007, resp.). In addition, PIO markedly inhibited DES-enhanced NF-κB function and DES-blocked PPAR- activity. Mechanically, DES induced PPAR- ubiquitination and degradation in protein level, which can be totally reversed by PIO. Conclusion. PIO treatment attenuated DES-induced PPAR loss, NF-κB activation, and proinflammation, indicating that PIO may have a novel direct protective role in modulating proinflammation in DES era.