2017
DOI: 10.4158/ep161445.ra
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Triglycerides, Atherosclerosis, and Cardiovascular Outcome Studies: Focus on Omega-3 Fatty Acids

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Cited by 42 publications
(19 citation statements)
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“…These studies, the first done in human cell and tissue models, support prior work done in animal in vivo and in vitro models documenting inflammation reducing effects of LC N-3 PUFA as well as changes in lipid droplet formation. Though data on the clinical use of LC N-3 PUFA in human metabolic disease, such as atherosclerosis and diabetes are conflicting [47][48][49][50][51][52], the pre-clinical evidence suggests there may be beneficial effects in the chronic inflammatory state of obesity.…”
Section: Discussionmentioning
confidence: 99%
“…These studies, the first done in human cell and tissue models, support prior work done in animal in vivo and in vitro models documenting inflammation reducing effects of LC N-3 PUFA as well as changes in lipid droplet formation. Though data on the clinical use of LC N-3 PUFA in human metabolic disease, such as atherosclerosis and diabetes are conflicting [47][48][49][50][51][52], the pre-clinical evidence suggests there may be beneficial effects in the chronic inflammatory state of obesity.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, triglycerides are an independent predictor of endothelial function which associated with atherosclerosis. It has been reported that raising-triglyceride increase clinical cardiovascular endpoints but lowering circulating triglyceride levels may improve endothelial function, leading to a decrease in cardiovascular events [ 28 30 ]. It has been reported that TG may also stimulate atherogenesis by producing proinflammatory cytokines, fibrinogen and coagulation factors.…”
Section: Discussionmentioning
confidence: 99%
“…rHDL were used in patients with acute coronary syndrome and lead to an increase in plasma HDL-C and a decrease in a decrease in LDL-C ( Chenevard et al, 2012 ). As a caveat to these positive findings, animal studies and HDL-targeted gene therapy studies have indicated that apoAI overexpression did not cause regression of pre-existing atherosclerotic lesions but rather retarded further expansion of pre-existing lesions ( Rong et al, 2001 ; Li et al, 2011 ; Van Craeyveld et al, 2011 ). Additionally, a study analyzing CER-001 found no difference between placebo and treatment in the reduction of atheroma volume ( Tardif et al, 2014 ).…”
Section: Novel Therapy To Target Protective Hdl Subclassmentioning
confidence: 99%