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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Actins, Angiotensin II, Animals, Atrial Natriuretic Factor, Body Weight, Cardiomegaly, Cell Size, Cells, Cultured, Chromans, Disease Models, Animal, Gene Expression, Heart, Heterozygote, Hypoglycemic Agents, Ligands, Mice, Mice, Knockout, Myocardium, Organ Size, Pioglitazone, Rats, Rats, Wistar, Receptors, Cytoplasmic and Nuclear, Rosiglitazone, Thiazoles, Thiazolidinediones, Transcription Factors, Troglitazone.
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Does peroxisome proliferator-activated receptor gamma play a critical role in inhibition of cardiac hypertrophy in vitro and in vivo? Context: 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. 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.
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These results suggest that the PPARgamma-dependent pathway is critically involved in the inhibition of cardiac hypertrophy. Final Decision: yes