Beginning to Understand High-Density Lipoproteins

Santos‐Gallego, Carlos G.; Badimón, Juan J.; Rosenson, Robert S.

doi:10.1016/j.ecl.2014.08.001

Cited by 88 publications

(61 citation statements)

References 194 publications

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“…SAA also stimulates NF-κB activation and induces the expression of pro-atherosclerotic factors, such as ICAM-1, MCP-1, MMP-9 and tissue factor in macrophages 20 . Lastly, SAA displaces apoA-I from the surface of the HDL particle, thus generating free apoA-I, which is cleared faster by the kidney, thus potentially affecting the anti-atherogenic effect of HDL 21 . In addition to the effects on SAA, we observed a slight effect on circulating lipoproteins (i.e.…”

Section: Discussionmentioning

confidence: 99%

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

et al. 2016

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Section: Discussionmentioning

confidence: 99%

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

et al. 2016

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“…lncRNAs, although initially considered as genomic transcription noise, have been demonstrated to play pivotal roles in multiple biological processes and are increasingly recognized as contributors to the pathology of cancer, neurodegenerative diseases, diabetes, heart diseases, and inflammation. lncRNA can also be transported in the plasma by exosomes and HDL particles [14] in the same way as microRNA are also transported by HDL particles [15]. Previous studies have identified that lncRNAs play an important role in genome regulation and human disease, especially by influencing proliferation, cell apoptosis, and signaling pathways to impact the mechanisms of disease.…”

Section: Discussionmentioning

confidence: 99%

Unraveling the Expression Profiles of Long Noncoding RNAs in Rat Cardiac Hypertrophy and Functions of lncRNA BC088254 in Cardiac Hypertrophy Induced by Transverse Aortic Constriction

Zhang²,

Liang³

2016

Cardiology

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Long noncoding RNAs (lncRNAs), although initially considered as genomic transcription noise, have been demonstrated to play pivotal roles in multiple biological processes and are increasingly recognized as contributors to the pathology of cancer, neurodegenerative diseases, diabetes, heart diseases, and inflammation. However, studies on the roles of lncRNAs in angiocardiopathy, particularly in cardiac hypertrophy, are still preliminary. In our study, differentially expressed lncRNAs in rat cardiac hypertrophy induced by transverse aortic constriction (TAC) were identified by microarray analysis and validated using quantitative real-time polymerase chain reaction (RT-PCR). Briefly, we identified 6,969 lncRNAs, among which 80 lncRNAs were significantly upregulated and 172 lncRNAs were significantly downregulated. Quantitative RT-PCR was used to validate the differential expression of 5 lncRNAs in myocardial tissue RNA. Further, pathway analysis indicated that 25 pathways corresponded to upregulated transcripts and 20 pathways corresponded to downregulated transcripts. Third, by coexpression network analysis, we found a correlation between BC088254 and phb2 (prohibitin 2) and verified this expression by RT-PCR and Western blot. This is the first study to reveal differentially expressed lncRNAs in rat cardiac hypertrophy induced by TAC, indicating potential lncRNA mechanisms of action in myocardial hypertrophy. We also found that lncRNA BC088254 may have a certain role in myocardial hypertrophy induced by TAC and functional relevance between lncRNA BCO88254 and phb2, but the relationship between these two factors is unclear.

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“…EL, Lp-PLA 2 ) [55][56][57]. Depending on the intervention, there may be large variations in the magnitude of the changes observed between the various HDL measures [58]. In some instances, the major effect of the intervention may be redistribution among HDL subclasses, with the total levels of any measure minimally affected.…”

Section: Implications Of Hdl-directed Therapiesmentioning

confidence: 99%

Underappreciated Opportunities for High-Density Lipoprotein Particles in Risk Stratification and Potential Targets of Therapy

Rosenson

Davidson

et al. 2015

Cardiovasc Drugs Ther

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The inverse relationship between high-density lipoprotein cholesterol (HDL-C) concentrations and coronary heart disease risk is well established. As a result, in recent years there have been significant resources focused on identifying therapies that raise HDL-C and ultimately reduce cardiovascular events. Unfortunately, a number of trials aimed at increasing HDL-C have failed to show improved outcomes, and hence, have cast doubt on the importance of HDL-C as a therapeutic target. HDL-C, however, is only one measure of HDL. HDL levels can also been estimated by quantifying apolipoprotein A-I (apoA-I) levels using enzyme immunoassay or by measuring HDL particle number (HDL-P) using nuclear magnetic resonance spectroscopy (NMR) or ion mobility. While these surrogate measures are correlated, they are not comparable. Lipoprotein-altering therapies have been shown to have different effects on HDL-C, apoA-I and HDL-P and several studies have demonstrated that HDL-P is a stronger predictor of coronary heart disease risk than HDL-C and/or apoA-I. This paper will review available evidence supporting the use of HDL-P as the biomarker of choice to assess the contribution of HDL to cardiovascular risk and as the primary goal of HDL-raising therapies.

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Beginning to Understand High-Density Lipoproteins

Cited by 88 publications

References 194 publications

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

Orthopedic surgery increases atherosclerotic lesions and necrotic core area in ApoE−/− mice

Unraveling the Expression Profiles of Long Noncoding RNAs in Rat Cardiac Hypertrophy and Functions of lncRNA BC088254 in Cardiac Hypertrophy Induced by Transverse Aortic Constriction

Underappreciated Opportunities for High-Density Lipoprotein Particles in Risk Stratification and Potential Targets of Therapy

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