Treatment of Pulmonary Arterial Hypertension With the Selective Endothelin-A Receptor Antagonist Sitaxsentan

Barst, Robyn J.; Langleben, David; Badesch, David B.; Frost, Adaani E.; Lawrence, E. Clinton; Shapiro, Shelley; Naeije, Robert; Galiè, Nazzareno

doi:10.1016/j.jacc.2006.01.057

Cited by 443 publications

(305 citation statements)

References 15 publications

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“…The critical role of ET-1 in PH has been largely demonstrated [20][21][22], underlying the now widely used therapeutic strategies in idiopathic PH based on ET-1 receptor blocking either dually [33,34] or specifically directed to ETAR [35]. Very few data other than increased ET-1 levels in serum [18] and in sputum [19] of CF patients exist as to a potentially pathogenic role of ET-1 in CF.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary vascular dysfunction in end-stage cystic fibrosis: role of NF-κB and endothelin-1

Henno¹,

Maurey²,

Danel³

et al. 2009

Eur Respir J

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Pulmonary hypertension is rare in chronic respiratory diseases but has a strong impact on the prognosis and is partly underlined by factors other than hypoxaemia. The aim of the present study was to assess the potential role of endothelin-1 (ET-1) and nuclear factor (NF)-kB vasoconstrictive pathways in pulmonary hypertension.The effects of ET-1 receptors blockers (BQ 123 and 788) and of genistein were assessed on response to acetylcholine of pulmonary vascular rings from cystic fibrosis (CF) lung transplant recipients (n523). NF-kB and ET-1 receptor expression was immunodetected in pulmonary arteries and quantitated using Western blotting. ET-1 vascular content was quantitated using ELISA.In total, 14 out of 23 subjects exhibited strongly impaired pulmonary vasodilation (p,0.01 versus nine out of 23 subjects with a normal response) associated with an activation of ET-1 receptors A and NF-kB pathways. Genistein restored vasodilation in subjects with an abnormal response.Pulmonary vascular dysfunction is frequent in end-stage CF, involving the NF-kB pathway and that of ET-1 through ET-1 receptor A (ETAR). These data leave a conceptual place for ETAR blockers and isoflavones in the management of the devastating vascular complication of chronic obstructive respiratory diseases such as CF.

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Section: Discussionmentioning

confidence: 99%

Pulmonary vascular dysfunction in end-stage cystic fibrosis: role of NF-κB and endothelin-1

Henno¹,

Maurey²,

Danel³

et al. 2009

Eur Respir J

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“…15,16,60 In clinic, efficacy and safety of endothelin-receptor antagonist has been confirmed in PAH patients. [61][62][63][64] Because ET-1 (upregulated in PAH) activates NFATc1, which in turn increases bcl ¡ 2 expression, contributing to the prosurvival and antiapoptotic effects of ET-1, 65 endothelin-receptor antagonist might also inhibit NFAT activation. At present, most of studies found that interventions targeting NFAT pathway may be effective for PAH therapy.…”

Section: Targeting the Nfat Pathway For Pah Therapymentioning

confidence: 99%

The role of nuclear factor of activated T cells in pulmonary arterial hypertension

et al. 2017

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Nuclear factor of activated T cells (NFAT) was first identified as a transcription factor about 3 decades ago and was not well studied until the development of immunosuppressant. Numerous studies confirm that calcineurin/NFAT signaling is very important in the development of vasculature and cardiovascular system during embryogenesis and is involved in the development of vascular diseases such as hypertension, atherosclerosis and restenosis. Recent studies demonstrated that NFAT proteins also regulate immune response and vascular cells in the pulmonary microenvironment. In this review, we will discuss how different NFAT isoforms contribute to pulmonary vascular remodeling and potential new therapeutic targets for treating pulmonary arterial hypertension.

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“…These drugs can improve the cardiac and pulmonary pressures as well as exercise capacity. [15][16][17] …”

Section: Endothelin-1 Receptor Antagonistsmentioning

confidence: 99%

Under Pressure: Pulmonary Arterial Hypertension . . . A Mother's Struggle

Weber¹,

Silver²,

Cromer³

et al. 2011

Critical Care Nurse

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Treatment of Pulmonary Arterial Hypertension With the Selective Endothelin-A Receptor Antagonist Sitaxsentan

Abstract: Treatment with the selective ET(A) receptor antagonist sitaxsentan, orally once daily at a dose of 100 mg, improves exercise capacity and WHO FC in PAH patients, with a low incidence of hepatic toxicity.

Cited by 443 publications

References 15 publications

Pulmonary vascular dysfunction in end-stage cystic fibrosis: role of NF-κB and endothelin-1

Pulmonary vascular dysfunction in end-stage cystic fibrosis: role of NF-κB and endothelin-1

The role of nuclear factor of activated T cells in pulmonary arterial hypertension

Under Pressure: Pulmonary Arterial Hypertension . . . A Mother's Struggle

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