2017
DOI: 10.11603/ijmmr.2413-6077.2017.2.7935
|View full text |Cite
|
Sign up to set email alerts
|

Endothelial Dysfunction and Cardiovascular Risk in Patients With Ankylosing Spondylitis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

0
1
0
1

Year Published

2023
2023
2023
2023

Publication Types

Select...
3

Relationship

0
3

Authors

Journals

citations
Cited by 3 publications
(2 citation statements)
references
References 6 publications
0
1
0
1
Order By: Relevance
“…In particular, Y. Li et al [9] have demonstrated the role of ED in the development and progression of AH by reducing the release of nitric oxide (NO) and acceleration of its degradation was proven, in addition to increased activity of angiotensin -converting enzyme on the surface of endothelial cells and increased synthesis of endothelin-1 and other vasoconstrictor substances by endothelial cells in case of their dysfunction. Chronic inhibition of NO in the experiment leads to all organic outcomes of severe long-lasting AH, including atherosclerosis and vascular organ damage [10]. Conversely, according to the research of J. Goodwin [11], high BP potentiates the escalation of oxidative stress and intracellular accumulation of free radicals that adversely affect the function and cohesion of endothelial lining and is one of the pathogenetic links of ED.…”
Section: Methodsmentioning
confidence: 99%
“…In particular, Y. Li et al [9] have demonstrated the role of ED in the development and progression of AH by reducing the release of nitric oxide (NO) and acceleration of its degradation was proven, in addition to increased activity of angiotensin -converting enzyme on the surface of endothelial cells and increased synthesis of endothelin-1 and other vasoconstrictor substances by endothelial cells in case of their dysfunction. Chronic inhibition of NO in the experiment leads to all organic outcomes of severe long-lasting AH, including atherosclerosis and vascular organ damage [10]. Conversely, according to the research of J. Goodwin [11], high BP potentiates the escalation of oxidative stress and intracellular accumulation of free radicals that adversely affect the function and cohesion of endothelial lining and is one of the pathogenetic links of ED.…”
Section: Methodsmentioning
confidence: 99%
“…На сьогодення достовірно відомо, що наявність хронічного системного запалення є вагомим предиктором розвитку СС захворювань [6][7][8][9][10] внаслідок розвитку ендотеліальної дисфункції (ЕД), а в подальшому -атеросклерозу, атеротромбозу, ремоделювання судинної стінки та міокарда [11][12] що і є, відповідно, основною причиною значно вищих від загально популяційних випадків несприятливих загрозливих для життя станів.…”
unclassified