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Cardiovasc Toxicol ; 19(1): 1-12, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30448914

RESUMO

The endothelium is a thin innermost layer of flat cells which release various mediators including endothelin-1 (ET-1), prostanoids, von Willebrand factor (vWF) and endothelium-derived relaxing factor (EDRF; nitric oxide) to regulate vascular tone. Endothelial nitric oxide synthase (eNOS) is a key enzyme that generates nitric oxide (NO). NO maintains vascular homeostasis and cardiac functions by influencing major vascular protective properties such as anti-platelet, anti-proliferative, anti-migratory, antioxidant and anti-inflammatory action in vessels. Abnormal endothelial production and release of NO lead to vascular endothelial dysfunction (VED) and further leads to pathogenesis in myocardial and other tissues. Numerous pharmacological agents such as angiotensin-converting enzyme inhibitors, statins, calcium channel blockers, ET-1 receptor antagonists, insulin sensitizers, antioxidants and supplements like tetrahydrobiopterin, arginine and folate have been implicated in the treatment of VED, but their therapeutic potency was restricted due to some unavoidable adverse effects. The new era with advances in nanotechnology and its ability to target a specific disease, nano-medicine explored an innovative gateway for advanced therapy for VED. The present commentary reveals the various available, pipeline nano-medicine, their interaction with endothelium and in other associated pathological conditions and their delivery strategies for target-specific treatment of VED.


Assuntos
Fármacos Cardiovasculares/administração & dosagem , Doenças Cardiovasculares/tratamento farmacológico , Endotélio Vascular/efeitos dos fármacos , Nanomedicina/métodos , Nanopartículas , Tecnologia Farmacêutica/métodos , Animais , Fármacos Cardiovasculares/química , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Portadores de Fármacos , Composição de Medicamentos , Endotélio Vascular/metabolismo , Endotélio Vascular/fisiopatologia , Humanos , Transdução de Sinais/efeitos dos fármacos
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