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We also investigated its influence on proliferation in human pulmonary arterial smooth muscle cells. We thank Prof. Nick Morrell for providing all hPASMCs.This article was sent to R. Clinton Webb, Guest Editor, for review by expert referees, editorial decision, and final disposition.The online-only Data Supplement is available with this article at We have identified that metformin can reverse pulmonary hypertension in females through inhibition of aromatase and decrease of estrogen and its metabolites, this mechanism has not been reported in pulmonary hypertension previously.We report, for the first time, that aryl hydrocarbon receptor (AhR) is increased in female patient’s pulmonary arterial smooth muscle cells in comparison with nonpatient pulmonary arterial smooth muscle cells and metformin can decrease AhR.The ability of metformin to affect steroidogenesis to reverse pulmonary hypertension in females is extremely relevant as a gender bias exists in this disease.Given the importance of AhR in mediating toxicity, it is relevant to note that metformin can decrease levels of AhR and that AhR may be modulated by AMP-activated protein kinase in this disease.Our study shows that metformin may provide an alternative therapy for females with pulmonary arterial hypertension through its target of AMP-activated protein kinase and estrogen synthesis and metabolism. We report that metformin increases pAMPK, which can affect CRTC2 gene expression, and aromatase PII promoter activity. In PH, this is a novel mechanism which is highly relevant given the role of estrogen metabolites and estrogen synthesis in the disease. Group 2 refers to PH caused by lef… PAH is characterized by elevated pulmonary pressure (>25 mm Hg at rest), vascular remodeling, and occlusive pulmonary vascular lesions. Unauthorized The study also suggests a role for AhR in PH, which is worthy of further investigation.The precise role of estrogen, its formation and its metabolites, in PAH requires to be fully understood to understand why females are more susceptible to the disease. Furthermore, metformin is already in widespread use as an anticancer drug and well tolerated by patients and thus suggests a practical therapy for females with this devastating disease.We thank Dr Kristy Brown and Maria Docanto from Monash University, Australia for providing the PII promoter plasmid. Correspondence to Margaret R. MacLean, College of Medical, Veterinary and Life Sciences, Research Institute of Cardiovascular and Medical Sciences, Room 448, West Medical Bldg/Wolfson Link Bldg, University of Glasgow, Glasgow G12 8QQ, United Kingdom. We thank Marie Anne Ewart and Benoit Viollet for assistance in interpretation of the data. Introduction. Metformin had no effect on systemic blood pressure, plasma glucose levels, and no effect on cardiac output and heart rate, demonstrating that the observed effects are pulmonary specific and independent of glycemia. Inhibition of aromatase using anastrazole is protective in experimental pulmonary hypertension but whether metformin attenuates pulmonary hypertension through this mechanism remains unknown. A single dose of sugen combined with hypoxia followed by weeks of normoxia provides a refined model of PAH exhibiting high pulmonary pressures and occlusive pulmonary lesions (the sugen/hypoxic rat model [hereafter termed SuHx]).Wistar Kyoto adult (9 weeks) female (Harlan, United Kingdom) rats were divided into 3 groups (n=12 per group), control (with no PH induced), vehicle dosed (0.9% [wt/vol] NaCl in distilled water for 21 days) and metformin dosed. Animals were then dosed, daily (oral gavage) with vehicle or with metformin (100 mg/kg; dissolved in 0.9% [wt/vol] NaCl) postoperatively, once daily for a further 21 days). [])) More than 30 randomised controlled trials (RCTs) of treatments have been performed, and surgery for patients with chronic thromboembolic pulmonary hypertension … Pulmonary hypertension is hemodynamically defined as a mean pulmonary artery pressure greater than 25 mm Hg at rest or greater than 30 mm Hg during exercise with an increased pulmonary vascular resistance (1,2).This condition may be caused by a wide variety of disease entities with overlapping radiologic-histologic features. The latter 2 groups received a single dose of Sugen-5416 (20 mg/kg; Novartis, United Kingdom), before being placed in a hypobaric chamber (atmospheric pressure 550 mbar) for 2 weeks and then placed in normal room pressure (1013 mbar) for 3 weeks while PH developed. For example, AMPK activation can affect the cyclooxygenase pathway as well as the mTOR pathway, both known to be dysregulated in PAH.It is possible that all the therapeutic effects of metformin could be driven via its ability to increase AMPK, and this work is supported by other studies, which indicate AMPK to be protective in PHWe previously showed that aromatase inhibition was only effective in female hypoxic and SuHx rat models of PH, having no effect in male rats with PH.In summary, we have demonstrated metformin to be protective in PH in the rat SuHx model and antiproliferative in hPASMCs.

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