Editing Endothelial dysfunction (section)

=== Atherosclerosis ===
[[File:Atherosclerosis timeline - endothelial dysfunction.svg|thumb|Stages of endothelial dysfunction in atherosclerosis of arteries]]
Endothelial dysfunction may be involved in the development of [[atherosclerosis]]<ref name="jh">{{cite journal|pmid=29664811|year=2018|last1=Maruhashi|first1=T|title=Assessment of endothelium-independent vasodilation: From methodology to clinical perspectives|journal=Journal of Hypertension|volume=36|issue=7|pages=1460–1467|last2=Kihara|first2=Y|last3=Higashi|first3=Y|doi=10.1097/HJH.0000000000001750|s2cid=4948849}}</ref><ref name="pmid24222847">{{cite journal | vauthors = Eren E, Yilmaz N, Aydin O | title = Functionally defective high-density lipoprotein and paraoxonase: a couple for endothelial dysfunction in atherosclerosis | journal = Cholesterol | volume = 2013 | pages = 792090 | date = 2013 | pmid = 24222847 | pmc = 3814057 | doi = 10.1155/2013/792090 | doi-access = free }}</ref><ref name="botts-2021">{{cite journal | vauthors = Botts SR, Fish JE, Howe KL | title = Dysfunctional Vascular Endothelium as a Driver of Atherosclerosis: Emerging Insights Into Pathogenesis and Treatment | journal = Frontiers in Pharmacology | volume = 12 | pages = 787541 | date = December 2021 | pmid = 35002720 | pmc = 8727904 | doi = 10.3389/fphar.2021.787541 | doi-access = free }}</ref> and may predate vascular pathology.<ref name=jh/><ref name="pmid18382884">{{cite journal | vauthors = Münzel T, Sinning C, Post F, Warnholtz A, Schulz E | title = Pathophysiology, diagnosis and prognostic implications of endothelial dysfunction | journal = Annals of Medicine | volume = 40 | issue = 3 | pages = 180–96 | date = 2008 | pmid = 18382884 | doi = 10.1080/07853890701854702 | s2cid = 18542183 | doi-access = free }}</ref> Endothelial dysfunction may also lead to increased adherence of [[monocyte]]s and [[macrophage]]s, as well as promoting infiltration of [[low-density lipoprotein]] (LDL) in the vessel wall.<ref>{{Cite journal |last=Poredos |first=P. |date=2001 |title=Endothelial dysfunction in the pathogenesis of atherosclerosis |url=https://pubmed.ncbi.nlm.nih.gov/11697708/ |journal=Clinical and Applied Thrombosis/Hemostasis|volume=7 |issue=4 |pages=276–280 |doi=10.1177/107602960100700404 |issn=1076-0296 |pmid=11697708|s2cid=71334997 }}</ref> [[Low-density lipoprotein#Oxidized LDL|Oxidized LDL]] is a hallmark feature of atherosclerosis,<ref name="pmid25804383" /> by promoting the formation of [[foam cell]]s, [[monocyte]] [[chemotaxis]], and platelet activation, leading to [[Atheroma|atheromatous plaque]] instability and ultimately to rupture.<ref name="pmid35722128">{{cite journal | vauthors = Jiang M, Zhou Y, Ge J | title=Mechanisms of Oxidized LDL-Mediated Endothelial Dysfunction and Its Consequences for the Development of Atherosclerosis | journal= [[Frontiers in Cardiovascular Medicine]] | volume=9 | pages=925923 | year=2022 | doi= 10.3389/fcvm.2022.925923 | pmc=9199460 | pmid=35722128 | doi-access=free }}</ref> [[Dyslipidemia]] and [[hypertension]] are well known to contribute to endothelial dysfunction,<ref>{{Cite journal |last1=Le Master |first1=Elizabeth |last2=Levitan |first2=Irena |date=2019-01-22 |title=Endothelial stiffening in dyslipidemia |journal=Aging |volume=11 |issue=2 |pages=299–300 |doi=10.18632/aging.101778 |issn=1945-4589 |pmc=6366977 |pmid=30674709}}</ref><ref>{{Cite book |last1=Konukoglu |first1=Dildar |last2=Uzun |first2=Hafize |chapter=Endothelial Dysfunction and Hypertension |date=2017 |title=Hypertension: From basic research to clinical practice |url=https://pubmed.ncbi.nlm.nih.gov/28035582/ |series=Advances in Experimental Medicine and Biology |volume=956 |pages=511–540 |doi=10.1007/5584_2016_90 |issn=0065-2598 |pmid=28035582|isbn=978-3-319-44250-1 }}</ref> and lowering blood pressure and LDL has been shown to improve endothelial function, particularly when lowered with [[ACE inhibitor]]s, [[calcium channel blocker]]s, and [[statin]]s.<ref name="pubmed.ncbi.nlm.nih.gov">{{Cite journal |last1=Ghiadoni |first1=Lorenzo |last2=Taddei |first2=Stefano |last3=Virdis |first3=Agostino |date=2012 |title=Hypertension and endothelial dysfunction: therapeutic approach |url=https://pubmed.ncbi.nlm.nih.gov/22112351/#:~:text=A%20large%20body%20of%20evidence%20indicates%20that%20patients,changes%20and%20can%20also%20contribute%20to%20cardiovascular%20events. |journal=Current Vascular Pharmacology |volume=10 |issue=1 |pages=42–60 |doi=10.2174/157016112798829823 |issn=1875-6212 |pmid=22112351}}</ref> Steadily laminar flow with high shear stress in blood vessels protects against atherosclerosis, whereas disturbed flow promotes atherosclerosis.<ref name="pmid31354915" />