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A host of causes may induce endothelial injury and TMA, including enteric bacterial toxins, deficiency or dysfunction of complement regulatory proteins, deficiency or inhibition of von Willebrand factor cleaving proteases, and factors that inhibit endothelial cell proliferation and turnover.
Several observations suggest that endothelial function is abnormal in migraine patients, including an increased prevalence of anti-endothelial cell antibodies that may induce endothelial damage and raised plasma levels of ET-1 and von Willebrand factor [29].
IL-17A may induce endothelial inflammation in SSc [ 15].
Exosomes from different vascular cells may induce endothelial cell apoptosis and thereby contribute to vascular dysfunction.
Several mechanisms may explain how lipid infusion may induce endothelial activation and eventual damage.
It is known that endothelial dysfunction occurs postprandially and that postprandial hyperglycemic spikes may induce endothelial dysfunction.
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Furthermore, recent in vitro and in vivo experimental data showed that apoCIII may directly induce endothelial dysfunction via inhibition of insulin-induced activation of Akt resulting in reduced nitric oxide (NO) release and subsequent impaired vasodilation [ 40].
Lead exposure may also induce endothelial injury and atherosclerosis [ 7– 9].
Resistin may also induce endothelial dysfunction [ 19, 20, 49] and treatment of macrophages with resistin could induce lipid accumulation, supporting further resistin's role in atherosclerosis [ 50].
Given the marked increase also seen in angiotensin II, there is interesting, albeit limited, evidence that both vasopressin and angiotensin may induce endothelin release from in vitro endothelial cells [ 167].
Even though widely used, excessive hypochlorite may induce neurodegeneration, endothelial apoptosis, ocular irritation, and other tissue damage [24, 33 37].
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