| First Author | Asakawa M | Year | 2002 |
| Journal | Circulation | Volume | 105 |
| Issue | 10 | Pages | 1240-6 |
| PubMed ID | 11889020 | Mgi Jnum | J:103209 |
| Mgi Id | MGI:3608735 | Doi | 10.1161/hc1002.105225 |
| Citation | Asakawa M, et al. (2002) Peroxisome proliferator-activated receptor gamma plays a critical role in inhibition of cardiac hypertrophy in vitro and in vivo. Circulation 105(10):1240-6 |
| abstractText | BACKGROUND: Peroxisome proliferator-activated receptors (PPARs) are transcription factors of the nuclear receptor superfamily. It has been reported that the thiazolidinediones, which are antidiabetic agents and high-affinity ligands for PPARgamma, regulate growth of vascular cells. In the present study, we examined the role of PPARgamma in angiotensin II (Ang II)-induced hypertrophy of neonatal rat cardiac myocytes and in pressure overload-induced cardiac hypertrophy of mice. METHODS AND RESULTS: Treatment of cultured cardiac myocytes with PPARgamma ligands such as troglitazone, pioglitazone, and rosiglitazone inhibited Ang II-induced upregulation of skeletal alpha-actin and atrial natriuretic peptide genes and an increase in cell surface area. Treatment of mice with a PPARgamma ligand, pioglitazone, inhibited pressure overload-induced increases in the heart weight-to-body weight ratio, wall thickness, and myocyte diameter in wild-type mice and an increase in the heart weight-to-body weight ratio in heterozygous PPARgamma-deficient mice. In contrast, pressure overload-induced increases in the heart weight-to-body weight ratio and wall thickness were more prominent in heterozygous PPARgamma-deficient mice than in wild-type mice. CONCLUSIONS: These results suggest that the PPARgamma-dependent pathway is critically involved in the inhibition of cardiac hypertrophy. |
