The role of HDL in plaque stabilization and regression

Feig, Jonathan E.; Feig, Jessica L.; Dangas, George

doi:10.1097/mca.0000000000000408

Cited by 22 publications

(16 citation statements)

References 132 publications

(142 reference statements)

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“…Marginal inverse correlations of HDL with carotid lesion sizes have been observed in previous crosses ( Grainger et al 2017 ) ( Rowlan et al 2013a ). Together, these findings support the concept that HDL protects against atherosclerosis by inhibiting plaque growth ( Feig et al 2016 ) though there are conflicting reports ( Shah et al 2013 ) , ( Holmes et al 2015 ). Non-HDL cholesterol and triglyceride levels showed little or no association with either aortic or carotid lesion sizes in this cross.…”

Section: Discussionsupporting

confidence: 76%

Regional Variation in Genetic Control of Atherosclerosis in Hyperlipidemic Mice

Jones¹,

An²,

Shi³

et al. 2020

G3 Genes|Genomes|Genetics

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Atherosclerosis is a polygenic disorder that often affects multiple arteries. Carotid arteries are common sites for evaluating subclinical atherosclerosis, and aortic root is the standard site for quantifying atherosclerosis in mice. We compared genetic control of atherosclerosis between the two sites in the same cohort derived from two phenotypically divergent Apoe-null (Apoe-/-) mouse strains. Female F2 mice were generated from C57BL/6 (B6) and C3H/He (C3H) Apoe-/- mice and fed 12 weeks of Western diet. Atherosclerotic lesions in carotid bifurcation and aortic root and plasma levels of fasting lipids and glucose were measured. 153 genetic markers across the genome were typed. All F2 mice developed aortic atherosclerosis, while 1/5 formed no or little carotid lesions. Genome-wide scans revealed 3 significant loci on chromosome (Chr) 1, Chr15, 6 suggestive loci for aortic atherosclerosis, 2 significant loci on Chr6, Chr12, and 6 suggestive loci for carotid atherosclerosis. Only 2 loci for aortic lesions showed colocalization with loci for carotid lesions. Carotid lesion sizes were moderately correlated with aortic lesion sizes (r=0.303; p=4.6E-6), but they showed slight or no association with plasma HDL, non-HDL cholesterol, triglyceride, or glucose levels among F2 mice. Bioinformatics analyses prioritized Cryge as a likely causal gene for Ath30, Cdh6 and Dnah5 as causal genes for Ath22. Our data demonstrate vascular site-specific effects of genetic factors on atherosclerosis in the same animals and highlight the need to extend studies of atherosclerosis to sites beyond aortas of mice.

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Section: Discussionsupporting

confidence: 76%

Regional Variation in Genetic Control of Atherosclerosis in Hyperlipidemic Mice

Jones¹,

An²,

Shi³

et al. 2020

G3 Genes|Genomes|Genetics

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“…It is likely that HDL-C may act as cardiovascular health biomarkers. 33 This study shows that the risk of coronary atherosclerosis is correlated with serum levels of IFN-γ in obese subjects. This indicates that the determination of IFN-γ levels in obese atherosclerotic subjects may predict their potential risky as an important parameter in the early detection of developing coronary artery disease.…”

Section: Resultsmentioning

confidence: 67%

Estimation of interferon gamma and some inflammatory atherogenic biomarkers levels in obese coronary atherosclerotic patients

Abdulrahman

AL-Barzinji

2020

Zanco J. Med. Sci.

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Atherosclerosis, an underlying cause of cardiovascular disease, is responsible for around half of all deaths in the wide world. 1 Interferon gamma (IFN-γ) is a signature cytokine of Th1 cells that play a key role in the atherosclerosis process. 2 It has atheroma-promoting properties, and involved both in early and late stages of atherosclerosis by promoting the recruitment and activation of T cells and macrophages, leads to the production of proinflammatory cytokines. 3 Several immunohistochemical studies have discovered localization of IFN-γ in the atherosclerotic lesion. 4 Studies also report that the removal of IFN-γ or its receptors leads to a reduction in atherosclerosis. 5 Obesity is one of the vital risk factors for atherosclerosis and cardiometabolic syndrome. There is evidence that proinflammatory cytokine, including IFN-γ are overexpressed from adipose tissue. Various mechanisms have been suggested Background and objective: Coronary atherosclerosis is an inflammatory disease that may be caused by numerous factors. One of the most important factors is obesity; there are high concentrations of interferon gamma (IFN-γ) in obese patients. This study aimed to assess the levels of proinflammatory markers IFN-γ and high sensitive C-reactive protein (Hs-CRP) in obese coronary atherosclerotic patients and determine its correlation with lipid profiles. Methods: The present case-control study was carried out between December 2017 and May 2018 in the Cardiac Center-Surgical Specialty Hospital in Erbil city. It included 49 coronary atherosclerotic patients, 25 males and 24 females, and 39 controls. The sera were subjected to estimate of some inflammatory biomarkers including IFN-γ, Hs-CRP, and lipid profile such as total cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C), low-density lipoproteins cholesterol (LDL-C) and very low-density lipoproteins (VLDL-C). Results: Serum concentrations of IFN-γ and Hs-CRP in coronary atherosclerotic patients were increased significantly than controls (P = 0.031, P = 0.001), respectively. Indeed the same above results were seen in obese coronary atherosclerotic patients and controls than non-obese coronary atherosclerotic patients controls. The mean concentration of lipid profile in obese coronary atherosclerotic patients was decreased than non-obese coronary atherosclerotic patients and controls, with no significant differences (P ≥0.05). There was a weak negative significant correlation between IFN-γ and HDL-C in obese coronary atherosclerotic patients (r=-0.456; P = 0.040). Conclusion: Proinflammatory cytokine as IFN-γ played a vital role in the pathophysiology of obese atherosclerotic patients in combination with Hs-CRP and LDL-C, which could be used as predictors for progressive the disease.

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“…The higher the HDL, lower the plaque height and the lipid content of the whole plaque and its 1st mm, which could be related with the protective role ascribed to HDL in atherosclerotic disease [37]. Although HDL did not show (negative) association with plaque presence or atherosclerotic burden, higher the HDL level, lower the plaque vulnerability.…”

mentioning

confidence: 90%

“…However, there are few clinical interventional studies that causally link plasma HDL to decreased progression or to regression of atherosclerotic plaques, probably associated with the few therapeutic agents that selectively and strongly raise HDL. On the other hand, some studies have suggested that the HDL functional quality rather its levels are associated with the atherosclerotic disease [37].…”

mentioning

confidence: 99%

Carotid and Femoral Atherosclerotic Plaques in Asymptomatic and Non-Treated Subjects: Cardiovascular Risk Factors, 10-Years Risk Scores, and Lipid Ratios’ Capability to Detect Plaque Presence, Burden, Fibro-Lipid Composition and Geometry

Marin

Bia

Zócalo

2020

JCDD

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Carotid and/or femoral atherosclerotic plaques (AP) assessment through imaging studies is an interesting strategy for improving individual cardiovascular risk (CVR) stratification and cardiovascular disease (CVD) and/or events prediction. There is no consensus on who would benefit from image screening aimed at determining AP presence, burden, and characteristics. Aims: (1) to identify, in asymptomatic and non-treated subjects, demographic factors, anthropometric characteristics and cardiovascular risk factors (CRFs), individually or grouped (e.g., CVR equations, pro-atherogenic lipid ratios) associated with carotid and femoral AP presence, burden, geometry, and fibro-lipid content; (2) to identify cut-off values to be used when considering the variables as indicators of increased probability of AP presence, elevated atherosclerotic burden, and/or lipid content, in a selection scheme for subsequent image screening. Methods: CRFs exposure and clinical data were obtained (n = 581; n = 144 with AP; 47% females). Arterial (e.g., ultrasonography) and hemodynamic (central [cBP] and peripheral blood pressure; oscillometry/applanation tonometry) data were obtained. Carotid and femoral AP presence, burden (e.g., AP number, involved territories), geometric (area, width, height) and fibro-lipid content (semi-automatic, virtual histology analysis, grayscale analysis and color mapping) were assessed. Lipid profile was obtained. Lipid ratios (Total cholesterol/HDL-cholesterol, LDL-cholesterol/HDL-cholesterol, LogTryglicerides(TG)/HDL-cholesterol) and eight 10-years [y.]/CVR scores were quantified (e.g., Framingham Risk Scores [FRS] for CVD). Results: Age, 10-y./CVR and cBP showed the highest levels of association with AP presence and burden. Individually, classical CRFs and lipid ratios showed almost no association with AP presence. 10-y./CVR levels, age and cBP enabled detecting AP with large surfaces (˃p75th). Lipid ratios showed the largest association with AP fibro-lipid content. Ultrasound evaluation could be considered in asymptomatic and non-treated subjects aiming at population screening of AP (e.g., ˃ 45 y.; 10-y./FRS-CVD ˃ 5–8%); identifying subjects with high atherosclerotic burden (e.g., ˃50 y., 10-y./FRS-CVD ˃ 13–15%) and/or with plaques with high lipid content (e.g., LogTG/HDL ˃ 0.135).

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The role of HDL in plaque stabilization and regression

Cited by 22 publications

References 132 publications

Regional Variation in Genetic Control of Atherosclerosis in Hyperlipidemic Mice

Regional Variation in Genetic Control of Atherosclerosis in Hyperlipidemic Mice

Estimation of interferon gamma and some inflammatory atherogenic biomarkers levels in obese coronary atherosclerotic patients

Carotid and Femoral Atherosclerotic Plaques in Asymptomatic and Non-Treated Subjects: Cardiovascular Risk Factors, 10-Years Risk Scores, and Lipid Ratios’ Capability to Detect Plaque Presence, Burden, Fibro-Lipid Composition and Geometry

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