Abstract:
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.
journal_name
Circulationjournal_title
Circulationauthors
Asakawa M,Takano H,Nagai T,Uozumi H,Hasegawa H,Kubota N,Saito T,Masuda Y,Kadowaki T,Komuro Idoi
10.1161/hc1002.105225subject
Has Abstractpub_date
2002-03-12 00:00:00pages
1240-6issue
10eissn
0009-7322issn
1524-4539journal_volume
105pub_type
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