ArticlePflugers Archiv : European journal of physiology2007
Angiotensin type 1 (AT1) and type 2 (AT2) receptors mediate the increase in TGF-beta1 in thyroid hormone-induced cardiac hypertrophy.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 30 citations in OpenAlex.
- New aspects of endocrine control of atrial fibrillation and possibilities for clinical translation.Cardiovascular research · 2021Review
- Cardioprotective effect of thyroid hormone is mediated by AT2 receptor and involves nitric oxide production via Akt activation in mice.Heart and vessels · 2018Article
- AT1 receptor blockage impairs NF-κB activation mediated by thyroid hormone in cardiomyocytes.Pflugers Archiv : European journal of physiology · 2018Article
- Protective and Therapeutic Effects of Chinese Medicine Formula Jiajian Yunvjian on Experimental Cardiac Remodeling after Myocardial Infarction Induced by Coronary Artery Ligation.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Article
- Thyroid hormone stimulates NO production via activation of the PI3K/Akt pathway in vascular myocytes.Cardiovascular research · 2010Article
- Thyroid Hormone Increases TGF-beta1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors.International journal of endocrinology · 2010Article
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3 authors at 1 institution in 1 country.
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Abstract
Increased thyroid hormone (TH) levels are known to induce cardiac hypertrophy. Some studies have provided evidence for a functional link between angiotensin II (ANG II) and transforming growth factor beta1 (TGF-beta1) in the heart, both being able to also induce cardiac hypertrophy. However, the contribution of this growth factor activated directly by TH or indirectly by ANG II in cardiac hypertrophy development remains unknown. To analyze the possible role of TGF-beta1 in cardiac hypertrophy induced by TH and also to evaluate if the TGF-beta1 effect is mediated by ANG II receptors, we employed Wistar rats separated into control, hypothyroid (hypo) and hyperthyroid (T4 - 10) groups combined or not with ANG II receptor blockers (losartan or PD123319). Serum levels of T3 and T4, systolic pressure and heart rate confirmed the thyroid state of the groups. The T4 - 10 group presented a significant increase in cardiac TGF-beta1 levels; however, TGF-beta1 levels in the hypo group did not change in relation to the control. Inhibition of the increase in cardiac TGF-beta1 levels was observed in the groups treated with T4 in association with losartan or PD123319 when compared to the T4 - 10 group. These results demonstrate for the first time the TH-modulated induction of cardiac TGF-beta1 in cardiac hypertrophy, and that this effect is mediated by ANG II receptors.
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