Abstract
Endothelial cell dysfunction is emerging as the ultimate culprit for diverse cardiovascular diseases and cardiovascular complications in patients with chronic renal diseases, yet the definition of this new syndrome, its pathophysiology and therapy remain poorly defined. Here, we summarize some molecular mechanisms leading from hyperhomocysteinemia, elevated asymmetric dimethylarginine (ADMA) and advanced glycation end products (AGEs)-modified proteins to atherogenic endothelial phenotype and offer a model of endothelial dysfunction based on the interconnectedness of diverse functions.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis
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Arginine / analogs & derivatives*
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Arginine / metabolism
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Cardiovascular Diseases / etiology
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Cardiovascular Diseases / pathology
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Cardiovascular Diseases / physiopathology
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Cellular Senescence
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Endothelium, Vascular / pathology
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Endothelium, Vascular / physiopathology*
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Glycation End Products, Advanced / metabolism
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Humans
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Hyperhomocysteinemia / complications
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Hyperhomocysteinemia / physiopathology
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Kidney Diseases / complications
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Kidney Diseases / pathology
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Kidney Diseases / physiopathology
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Models, Biological
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Oxidative Stress
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Syndrome
Substances
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Glycation End Products, Advanced
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N,N-dimethylarginine
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Arginine