Foam cells in atherosclerosis

Yu, Xiaohua; Fu, Yue; Zhang, Da Wei; Yin, Kai; Tang, Chao-Ke

doi:10.1016/j.cca.2013.06.006

Cited by 642 publications

(523 citation statements)

References 81 publications

Supporting

Mentioning

506

Contrasting

Unclassified

Order By: Relevance

“…Meanwhile, ATP attenuated fat deposition in cardiac epicardium and reduced foam cells in thoracic aorta. It is well known that foam cell promotes the formation of fatty streak in blood vessels that is an early marker of atherosclerosis (Botham et al 2007;Yu et al 2013). It is generally accepted that total TG levels are an independent predictor for coronary heart diseases (Imke et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Antihyperlipidemic activity of adenosine triphosphate in rabbits fed a high-fat diet and hyperlipidemic patients

Zhang

Liang

Tong

et al. 2016

Pharmaceutical Biology

View full text Add to dashboard Cite

Context Recently, adenosine triphosphate (ATP) was occasionally found to decrease the triglyceride (TG) levels in several hyperlipidemic patients in our clinical practice. Objective The study investigates the anti-hyperlipidemic effects of ATP in a high-fat fed rabbit model and hyperlipidemic patients. Materials and methods Twenty-four rabbits were randomly divided into three groups of eight animals each as follows: normal diet, high-fat diet and high-fat diet + ATP group. ATP supplementation (40 mg/day) was started at the 20th day and lasted for 10 days. Serum concentrations of total cholesterol (TC), TG, LDL-C, HDL-C were measured on the 20th day and 30th day. Heart, liver and aorta were subjected histopathological examination. Twenty outpatients diagnosed primary hyperlipidemia took ATP at a dose of 60 mg twice a day for 1 week.Results Feeding rabbits with a high-fat diet resulted in a significant elevation of lipid parameters including TC, TG, LDL-C, VLDL-C compared to the normal diet group (p50.01). ATP treatment significantly decreased serum TG level (p50.01), whilst other parameters remained statistically unaltered. Meanwhile, ATP significantly reduced the thickness of fat layer in cardiac epicardium (p50.05) and pathological gradation of ballooning degeneration in hepatocytes (p50.05). After taking ATP for 1 week, hyperlipidemia patients exhibited a significant decrease of TG (p50.01), but other lipid parameters had no significant change. Discussion and conclusion The study indicates that ATP selectively decreases serum TG levels in high-fat diet rabbits and hyperlipidemic patients. Therefore, ATP supplementation may provide an effective approach to control TG level. ARTICLE HISTORY

show abstract

Section: Discussionmentioning

confidence: 99%

Antihyperlipidemic activity of adenosine triphosphate in rabbits fed a high-fat diet and hyperlipidemic patients

Zhang

Liang

Tong

et al. 2016

Pharmaceutical Biology

View full text Add to dashboard Cite

show abstract

“…Three types of carriers for cholesterol efflux have so far been identified, ABCA1, ABCG1 and SR-B1. ABCA1 mainly presents to apoA-I, while ABCG1 and SR-B1 present to mature HDL [32] . Recently, Fu et al [33] found that ABCA12 deficiency increased ABCA1 degradation, added to the accumulation of cholesterol in macrophages and the formation of foam cells and damaged the process of macrophage RCT, which resulted in the promotion of AS progression.…”

Section: Effects Of Macrophage Autophagy On Cholesterol Effluxmentioning

confidence: 99%

The roles of macrophage autophagy in atherosclerosis

Shao

Han

Zeng³

et al. 2016

Acta Pharmacol Sin

192

116

View full text Add to dashboard Cite

Although various types of drugs and therapies are available to treat atherosclerosis, it remains a major cause of mortality throughout the world. Macrophages are the major source of foam cells, which are hallmarks of atherosclerotic lesions. Consequently, the roles of macrophages in the pathophysiology of atherosclerosis are increasingly investigated. Autophagy is a self-protecting cellular catabolic pathway. Since its discovery, autophagy has been found to be associated with a variety of diseases, including cardiovascular diseases, malignant tumors, neurodegenerative diseases, and immune system disorders. Accumulating evidence demonstrates that autophagy plays an important role in inhibiting inflammation and apoptosis, and in promoting efferocytosis and cholesterol efflux. These facts suggest the induction of autophagy may be exploited as a potential strategy for the treatment of atherosclerosis. In this review we mainly discuss the relationship between macrophage autophagy and atherosclerosis and the molecular mechanisms, as well as the recent advances in targeting the process of autophagy to treat atherosclerosis.

show abstract

“…71 In macrophages and VSMCs derived from atherosclerotic plaques, ABCA1 expression and ApoA1-binding capacity is markedly reduced that in turn diminishes ApoA1-mediated cholesterol efflux and promotes lipid deposition. [71][72][73][74] Notably, as mentioned above, ApoA1 could be modified in atherosclerotic plaques through oxidation, nitration, and other mechanisms. This could greatly impair functional properties of intact ApoA1 and even make it dysfunctional.…”

Section: Role Of Modified Apoa1 In Atherosclerosismentioning

confidence: 99%