Histone Deacetylase 9 Represses Cholesterol Efflux and Alternatively Activated Macrophages in Atherosclerosis Development

Cao, Qiang; Rong, Shunxing; Repa, Joyce J.; Clair, R. St.; Parks, John S.; Mishra, Nilamadhab

doi:10.1161/atvbaha.114.303393

Cited by 159 publications

(142 citation statements)

References 38 publications

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“…A recent study found that targeted depletion of HDAC9 in bone marrow cells attenuates atherogenesis in LDLr −/− mice. 19 HDAC9 was further shown to repress cholesterol efflux in macrophages. However, whether the changes in macrophages give rise to atherosclerotic lesion formation remains speculative.…”

Section: January 2015mentioning

confidence: 99%

“…However, we cannot exclude skewing of macrophage polarization from M1 to M2 phenotype as previously reported. 19 The precise mechanisms by which increased HDAC9 expression promotes atherogenesis and vascular risk remain to be determined. A recent study found that targeted depletion of HDAC9 in bone marrow cells attenuates atherogenesis in LDLr −/− mice.…”

Section: January 2015mentioning

confidence: 99%

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Deficiency of the Stroke Relevant HDAC9 Gene Attenuates Atherosclerosis in Accord With Allele-Specific Effects at 7p21.1

Azghandi

Prell

Laan

et al. 2015

Stroke

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ApoE−/− mice exhibited markedly reduced lesion sizes throughout atherosclerotic aortas and significantly less advanced lesions. The proportion of Mac3-positive macrophages was higher in plaques from HDAC9 −/− ApoE −/− mice, but this was largely because of a lower proportion of advanced lesions. Analysis of human atherosclerotic plaques revealed no association between rs2107595 and specific plaque characteristics. Conclusions-Our results suggest that HDAC9 represents the disease-relevant gene at the stroke and coronary artery disease risk locus on 7p21.1, and that risk alleles in this region mediate their effects through increased HDAC9 expression. Targeted inhibition of HDAC9 might be a viable strategy to prevent atherosclerosis.

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Section: January 2015mentioning

confidence: 99%

Section: January 2015mentioning

confidence: 99%

Deficiency of the Stroke Relevant HDAC9 Gene Attenuates Atherosclerosis in Accord With Allele-Specific Effects at 7p21.1

Azghandi

Prell

Laan

et al. 2015

Stroke

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show abstract

“…[142][143][144][145][146][147] Identification and characterization of common epigenetic outcomes linked to disease manifestations and their interaction with nutrient status may allow the development of specific treatment and intervention measures. [148][149][150][151] Interestingly, the effect of limited or oversaturated nutrient bioavailability on epigenetic states is complex and not necessarily direct. For example, deficiency of methyl donors results in hypermethylation at some loci and hypomethylation at others.…”

Section: Role Of Nutrition In Epigenetic Perturbationmentioning

confidence: 99%

Nutrigenomics, the Microbiome, and Gene-Environment Interactions: New Directions in Cardiovascular Disease Research, Prevention, and Treatment

Ferguson¹,

Allayee²,

Gerszten³

et al. 2016

Circ Cardiovasc Genet

101

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Abstract-Cardiometabolic diseases are the leading cause of death worldwide and are strongly linked to both genetic and nutritional factors. The field of nutrigenomics encompasses multiple approaches aimed at understanding the effects of diet on health or disease development, including nutrigenetic studies investigating the relationship between genetic variants and diet in modulating cardiometabolic risk, as well as the effects of dietary components on multiple "omic" measures, including transcriptomics, metabolomics, proteomics, lipidomics, epigenetic modifications, and the microbiome. Here, we describe the current state of the field of nutrigenomics with respect to cardiometabolic disease research and outline a direction for the integration of multiple omics techniques in future nutrigenomic studies aimed at understanding mechanisms and developing new therapeutic options for cardiometabolic disease treatment and prevention. The interpretation and scope of nutrigenomics may vary, but it can be thought to encompass the spectrum of nutritional genomics research, including classic nutrigenetics studies of gene-diet interactions and molecular nutrition, in vitro and in vivo models, human nutrition studies, and the application of largescale, unbiased studies using high-throughput "omics" techniques to study the effects of nutrients on the body. 6 As the Figure shows, diet and the genome may influence cardiometabolic health through a variety of interconnected intermediates, perturbations in which can be measured through omics technologies, including RNA expression (transcriptome), epigenetic modifications (epigenome), metabolites (metabolome), lipids (lipidome), proteins (proteome), and resident microbial communities (microbiome). Although it is clear that both nutrients and genes play a distinct role in determining health, the complex interactions among genes, diet, and downstream networks are not well understood. The application of nutrigenomics approaches to questions of human health and disease is an important component in understanding the complexities of the interplay between basic metabolic processes and externalThe American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on January 22, 2016, and the American Heart Association Executive Committee on February 23, 2016. A copy of the document is available at http://professional.heart.org/statements by using either "Search for Guidelines & Statements" or the "Browse by Topic" area. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@ wolterskluwer.com.The...

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“…26 Moreover, overexpression of macrophage HDAC9 was reported to be atherogenic via inhibition of cholesterol efflux and the generation of alternatively activated macrophages. 27 However, the role of HDAC9 in atherosclerosis has not yet been fully elucidated.…”

Section: Effects Of Mir-182 On Hdac9mentioning

confidence: 99%

MicroRNA-182 Promotes Lipoprotein Lipase Expression and Atherogenesisby Targeting Histone Deacetylase 9 in Apolipoprotein E-Knockout Mice

Cheng

Gong

Zhao

et al. 2017

Circ J

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Histone Deacetylase 9 Represses Cholesterol Efflux and Alternatively Activated Macrophages in Atherosclerosis Development

Cited by 159 publications

References 38 publications

Deficiency of the Stroke Relevant HDAC9 Gene Attenuates Atherosclerosis in Accord With Allele-Specific Effects at 7p21.1

Deficiency of the Stroke Relevant HDAC9 Gene Attenuates Atherosclerosis in Accord With Allele-Specific Effects at 7p21.1

Nutrigenomics, the Microbiome, and Gene-Environment Interactions: New Directions in Cardiovascular Disease Research, Prevention, and Treatment

MicroRNA-182 Promotes Lipoprotein Lipase Expression and Atherogenesisby Targeting Histone Deacetylase 9 in Apolipoprotein E-Knockout Mice

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