| Causes of Scleroderma (MAIN MENU) |
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| Endothelin and Systemic Scleroderma |
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| Endothelin and Systemic Scleroderma |
| Endothelin and Systemic Scleroderma. Endothelin is a protein that helps to regulate contraction and relaxation of the smooth muscle found in the walls of blood vessels and internal organs (except the heart). An overproduction of endothelin, whether by illness or medication, can cause blood vessels to constrict and blood pressure to increase. In scleroderma, it can cause pulmonary arterial hypertension (PAH). ISN. |
| Endothelin. Endothelins are protein that constrict blood vessels and raise blood pressure. Among the strongest vasoconstrictors known, endothelins are implicated in vascular diseases of several organ systems, including the heart, general circulation and brain. Answers.com. |
| International conference on endothelin (ET). Identified in 1988, ET is produced by most tissues in the body. The protein is highly concentrated in the brain, lungs, kidney, heart, blood vessels and even in some cancer cells. ET is also the most potent vasoconstrictor (causing the blood vessels to constrict) known. Donna Krupa. EurekAlert. 09/10/09. |
| Raynaud’s Phenomenon and Plasma Endothelin (ET-1): Correlations with Capillaroscopic Patterns in Systemic Sclerosis (SSc). Highest ET-1 plasma levels were detected in the more advanced stage of the SSc microangiopathy, namely the late nailfold videocapillaroscopy pattern, characterized by capillary loss and increased tissue fibrosis; this might support the involvement of ET-1 in the progression of the microvascular/fibrotic SSc damage. Alberto Sulli. Journal of Rheumatology. June 2009, 36 (6). (Also see: Raynaud's) |
| When healing turns to scarring: Research reveals why it happens and how to stop it. During tissue repair, specialized cells called myofibroblasts migrate to the wound where they generate the adhesive and tensile forces required for wound closure. Normally, these myofibroblasts then disappear from the wound. But if they persist and continue to make connective tissue, it can become too thick, preventing the organ from functioning properly. EurekAlert! 09/18/08. (Also see: Causes of Scleroderma: Fibroblasts) |
| How does endothelial cell injury start? The role of endothelin in systemic sclerosis. This article reviews the role of endothelin as an example of a pleiotropic mediator with effects on various aspects of SSc pathogenesis, such as inflammation, vasculopathy and tissue remodelling. Arthritis Research & Therapy 2007, 9(Suppl 2):S2. |
| Systemic Sclerosis Patients Have Activating Antibodies Targeting Both Endothelin Receptor Type A And Angiotensin Ii Type 1 Receptor Predicting Worse Prognosis. Anti-AT1R and anti-ETAR antibodies are a biomarker for severe disease and worse prognosis and could explain pathogenic features found in systemic sclerosis. The detection of these antibodies could identify SSc patients that might benefit from a receptor blockade or from a specific modulation of the antibody-receptor interaction. G. Riemekasten OP0162 EULAR 2007. (Also see: Antibodies) |
| Endothelin and Autoimmunity |
| Elevated platelet-monocyte complexes (PMC) ın patıents wıth psorıatıc arthrıtıs (PsA). Endothelial activation might have a role in the pathogenesis of both psoriasis and PsA. Among parameters of platelet activation, only PMC might play a role in the pathogenesis of PsA. (InformaWorld) G.E. Pamuk. Platelets. September 14 2009. (Also see: Psoriasis) |
| Endothelin Receptor Antagonist (ETRA) |
| Endothelin Receptor Antagonists (ETRA). Endothelin receptor antagonists are a new class of drugs for the treatment of a number of major diseases, including pulmonary arterial hypertension. Endothelin receptor antagonists block endothelin receptors, thereby limiting harmful excess endothelin in the blood vessels. ETRAs include Letairis™ (Ambrisentan) and Tracleer® (Bosentan). PHCentral. August 2009. |
| Endothelin drugs benefit those with pulmonary hypertension. Recent research to block the effects of endothelin, a powerful substance that constricts blood vessels and stimulates cell growth, has led to successful treatment of pulmonary arterial hypertension and provides hope for treating other chronic diseases. Donna Krupa. EurekAlert. (GEN News). 09/10/09. (Also see: Pulmonary Hypertension) |
| Improved endothelial function after endothelin (ET(A)) receptor blockade in patients with systemic sclerosis (SSc). The results of this study suggest novel vasculoprotective effects of ET(A) receptor antagonism and support further exploration of strategies that target the endothelin 1 pathway in SSc. C. Cardillo. (PubMed) Arthritis Rheum. June 2009 (Also see: Vascular Involvement) |
| Simvastatin Reduces Endothelial Activation and Damage But Is Partially Ineffective in Inducing Endothelial Repair in Systemic Sclerosis (SSc). Treatment with simvastatin results in rapid and significant improvement of measures of endothelial activation, suggesting a potential role of statins in the treatment of peripheral vascular disease in SSc. Journal of Rheumatology. June 2008. (Also see: Medications and Raynaud's) |
