subendothelium

sub·en·do·the·li·um

(sŭb'en-dō-thē'lē-ŭm),
The connective tissue between the endothelium and inner elastic membrane in the intima of arteries.

sub·en·do·the·li·um

(sŭb'en-dō-thē'lē-ŭm)
The connective tissue between the endothelium and inner elastic membrane in the intima of arteries.

subendothelial

, subendothelium (sŭb″ĕn-dō-thē′lē-ăl) (sŭb″ĕn-dō-thē′lē-ŭm) [″ + Gr. endon, within, + thele, nipple]
Beneath the endothelium.
References in periodicals archive ?
Enhanced platelet adhesiveness to the subendothelium and higher protein exudation through vessel wall may promote atherosclerotic tendency.
The human umbilical cord is a promising source of MSCs, as MSCs can be isolated either from the whole umbilical cord [16,77], the umbilical vein subendothelium [78], or WJ [14, 19, 74].
Macrophages stimulated by the treatment of nicotine secrete elevated inflammatory cytokines, namely, tumor necrosis factor-[alpha] (TNF-[alpha]), IL-1[beta], and chemokines, creating the proinflammatory microenvironment in the subendothelium [23].
Gut microbe-derived TMAO could enforce the expression of the receptor of SR-A and CD36, which promotes the formation of foam cells whose accumulation within the subendothelium or neointima constitutes the first step in AS.
Pathologic diagnosis was based on the presence of all 3 of the following histologic signs: widening of subendothelium with myxoid degeneration, intraluminal thrombus formation, and fibrinoid necrosis of terminal arterioles.
The longer retention of sdLDL in subendothelium makes easier their modification by oxidation or the glycation, so their role in the development of endothelial dysfunction is usually attributed to oxidative modification and to the mechanisms of action of oxidised LDL (oxLDL) [47].
The other possible mechanisms are chemical arteritis and tissue destruction of endothelium, subendothelium, or muscle layers of vessel (1, 6, 7).
Morphological studies revealed that endothelium and subendothelium containing collagen fibers covered the graft completely and neointima was formed.
This interaction plays a key role in the initial adhesion of platelets to the subendothelium, which in turn induces a complex cascade of signals which results in platelet aggregation [47].
(22) Anemia could further worsen the bleeding disorder because red cells release ADP and facilitate platelets contacting with subendothelium at the damage site.
Migration of monocytes into the subendothelium is the initial step of inflammation and atherosclerotic plaque formation, which plays a key role in the atherosclerotic plaque formation.