Effect of anti-IL17 and/or Rho-kinase inhibitor treatments on vascular remodeling induced by chronic allergic pulmonary inflammation
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چکیده
منابع مشابه
Chronic Allergic Inflammation Causes Vascular Remodeling and Pulmonary Hypertension in Bmpr2 Hypomorph and Wild-Type Mice
Loss-of-function mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene have been identified in patients with heritable pulmonary arterial hypertension (PAH); however, disease penetrance is low, suggesting additional factors play a role. Inflammation is associated with PAH and vascular remodeling, but whether allergic inflammation triggers vascular remodeling in individuals wi...
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Pulmonary remodeling is an important feature of asthma physiopathology that can contribute to irreversible changes in lung function. Although neurokinins influence lung inflammation, their exact role in the extracellular matrix (ECM) remodeling remains to be determined. Our objective was to investigate whether inactivation of capsaicin-sensitive nerves modulates pulmonary ECM remodeling in anim...
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motility, migration, proliferation, differentiation, and apoptosis. Activation of Rho/ROCK is considered to play a major role in the pathogenesis of several cardiovascular diseases, including PH,5 and thus is a new therapeutic target for PH (Figure). Fasudil is one of the most frequently used ROCK inhibitors, and was approved as a therapeutic agent for vasospasm after arachnoid hemorrhage. Seve...
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متن کاملAllergic lung inflammation induces pulmonary vascular hyperresponsiveness.
Pulmonary arterial vasoconstriction is an important early component of pulmonary hypertension. Inflammatory mechanisms play a prominent role in the pathogenesis of pulmonary hypertension. The present authors investigated the potential role of acute allergic lung inflammation for alterations in pulmonary haemodynamics. BALB/c mice were intraperitoneally sensitised to ovalbumin and challenged by ...
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ژورنال
عنوان ژورنال: Therapeutic Advances in Respiratory Disease
سال: 2020
ISSN: 1753-4666,1753-4666
DOI: 10.1177/1753466620962665