Vascular endothelium dysfunction: a conservative target in metabolic disorders

Aim Vascular endothelium plays a role in capillary transport of nutrients and drugs and regulates angiogenesis, homeostasis, as well as vascular tone and permeability as a major regulator of local vascular homeostasis. The present study has been designed to investigate the role of endothelium in met...

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Vydané v:	Inflammation research Ročník 67; číslo 5; s. 391 - 405
Hlavní autori:	Jamwal, Shalini, Sharma, Saurabh
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Cham Springer International Publishing 01.05.2018 Springer Nature B.V
Predmet:	Aldehyde reductase Allergology Angiogenesis Angiotensin Angiotensin II Animals Anions Arginine Bioavailability Biomedical and Life Sciences Biomedicine Cardiovascular Diseases - physiopathology Cardiovascular Diseases - therapy Cholesterol Cytokines Dephosphorylation Dermatology Diabetes Diabetes mellitus Disorders Drugs Endothelium Endothelium, Vascular - physiopathology Glycosylation Homeostasis Homocysteine Humans Hypercholesterolemia Hyperhomocysteinemia Hypertension Immunology Inflammation Kinases Metabolic Diseases - complications Metabolic Diseases - therapy Metabolic disorders Molecular modelling Monomethyl-L-arginine Neurology Nitric oxide Nutrients Oxidation Oxidative stress Permeability Peroxides Pharmacology/Toxicology Phosphorylation Prostaglandins Protein kinase Reactive oxygen species Review Rheumatology Vascular Diseases - etiology Vascular Diseases - physiopathology Vascular Diseases - therapy Vasoconstriction Vasodilation Xanthine oxidase Vascular endothelial dysfunction Hypertension Endothelial Oxidative stress Cardiovascular disease Nitric oxide
ISSN:	1023-3830, 1420-908X, 1420-908X
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Shrnutí:	Aim Vascular endothelium plays a role in capillary transport of nutrients and drugs and regulates angiogenesis, homeostasis, as well as vascular tone and permeability as a major regulator of local vascular homeostasis. The present study has been designed to investigate the role of endothelium in metabolic disorders. Methods The endothelium maintains the balance between vasodilatation and vasoconstriction, procoagulant and anticoagulant, prothrombotic and antithrombotic mechanisms. Results Diabetes mellitus causes the activation of aldose reductase, polyol pathway and advanced glycation-end-product formation that collectively affect the phosphorylation status and expression of endothelial nitric oxide synthatase (eNOS) and causes vascular endothelium dysfunction. Elevated homocysteine levels have been associated with increase in LDL oxidation, generation of hydrogen peroxides, superoxide anions that increased oxidative degradation of nitric oxide. Hyperhomocysteinemia has been reported to increase the endogenous competitive inhibitors of eNOS viz L-N-monomethyl arginine (L-NMMA) and asymmetric dimethyl arginine (ADMA) that may contribute to vascular endothelial dysfunction. Hypercholesterolemia stimulates oxidation of LDL cholesterol, release of endothelins, and generation of ROS. The increased cholesterol and triglyceride level and decreased protective HDL level, decreases the activity and expression of eNOS and disrupts the integrity of vascular endothelium, due to oxidative stress. Hypertension also stimulates release of endothelins, vasoconstrictor prostanoids, angiotensin II, inflammatory cytokines, xanthine oxidase and, thereby, reduces bioavailability of nitric oxide. Conclusion Thus, the cellular and molecular mechanisms underlying diabetes mellitus, hyperhomocysteinemia, hypercholesterolemia hypertension and hyperuricemia leads to an imbalance of phosphorylation and dephosphorylation status of lipid and protein kinase that cause modulation of vascular endothelial L-arginine/nitric oxide synthetase (eNOS), to produce vascular endothelium dysfunction.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Literature Review-3 ObjectType-Review-3 content type line 23
ISSN:	1023-3830 1420-908X 1420-908X
DOI:	10.1007/s00011-018-1129-8