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Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis
Open accessAbstract
Plasma HDL levels have a protective role in atherosclerosis, yet clinical therapies to raise HDL levels have remained elusive. Recent advances in the understanding of lipid metabolism have revealed that miR-33, an intronic microRNA located within the SREBF2 gene, suppresses expression of the cholesterol transporter ABC transporter A1 (ABCA1) and lowers HDL levels. Conversely, mechanisms that inhibit miR-33 increase ABCA1 and circulating HDL levels, suggesting that antagonism of miR-33 may be atheroprotective. As the regression of atherosclerosis is clinically desirable, we assessed the impact of miR-33 inhibition in mice deficient for the LDL receptor (Ldlr-/- mice), with established atherosclerotic plaques. Mice treated with anti-miR33 for 4 weeks showed an increase in circulating HDL levels and enhanced reverse cholesterol transport to the plasma, liver, and feces. Consistent with this, anti-miR33-treated mice showed reductions in plaque size and lipid content, increased markers of plaque stability, and decreased inflammatory gene expression. Notably, in addition to raising ABCA1 levels in the liver, anti-miR33 oligonucleotides directly targeted the plaque macrophages, in which they enhanced ABCA1 expression and cholesterol removal. These studies establish that raising HDL levels by anti-miR33 oligonucleotide treatment promotes reverse cholesterol transport and atherosclerosis regression and suggest that it may be a promising strategy to treat atherosclerotic vascular disease.
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“Furthermore, macrophages within the atherosclerotic lesions of these mice exhibit an anti-inflammatory phenotype characterized by enhanced cholesterol efflux, which leads to a reduction in foam cell formation.”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [21]
In the citing paper
“Inhibition or genetic ablation of miR-33a has been shown to either promote the regression of atherosclerosis or prevent its formation in mouse models, such as LDL receptor-deficient or apoprotein E (ApoE)-deficient mice, conferring resistance to the disease 21 - 23) .”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [21]
In the citing paper
“Moreover, the effect of miR-33 deletion in macrophages is not as simple as the shift from the M1 to M2 phenotype reported previously.19”
From MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE −/− Mice (2012) · cites this paper as [19]
In the citing paper
“Moreover, antisense inhibition of miR-33 resulted in a regression of the atherosclerotic plaque volume in LDL-receptor-deficient mice.19”
From MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE −/− Mice (2012) · cites this paper as [19]
In the citing paper
“In any case, the effect of miR-33 deletion in macrophages is not as simple as a shift from the M1 to the M2 phenotype, as described in a previous report.19”
From MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE −/− Mice (2012) · cites this paper as [19]
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The Therapeutic Potential of MicroRNAs in Cancer
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“miR-33a/b-5p Mouse, monkey LDLR–/–; Western diet, ↑ High carb/moderate cholesterol AntimiR-33 reduces atherogenic plaques, increases plasma HDL (130, 174) (132)”
BackgroundNon-Coding RNA-Targeted Therapy: A State-of-the-Art Review
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“Further, among the downstream effects of SIRT1 activation is the enhanced expression of the cholesterol transporter ATPbinding cassette, subfamily A, member 1 (ABCA1), which is also post-transcriptionally targeted by miR-33 (79,121).”
BackgroundmiR-33-5p, a novel mechano-sensitive microRNA promotes osteoblast differentiation by targeting Hmga2
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“We have previously shown that Abca1 and Abcg1 mRNAs are both targets of miR33(10) and that treatment of Ldlr/ mice with anti-miR33 upregulated ABCA1 in the liver and macrophages and resulted in plaque regression.(9) Taken with our findings that both Abca1 and Abcg1 are downregulated by hyperglycemia,(11) which may con…”
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Paradoxical Suppression of Atherosclerosis in the Absence of microRNA-146a
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Javadifar, A., Rastgoo, S., Banach, M., Jamialahmadi, T., Johnston, T., & Sahebkar, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22052529 · Cited by 89
MicroRNA Control of High-Density Lipoprotein Metabolism and Function
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“atherosclerotic plaque macrophages to reduce plaque cholesterol content.(78) Although miR-33 has been the most extensive-”
Self-citationMicroRNA Modulation of Cholesterol Homeostasis
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“miR-33 inhibition increased circulating HDL-cholesterol levels and hepatic ABCA1 expression in both mice and monkeys (188, 189).”
BackgroundInhibition of atherosclerosis-promoting microRNAs via targeted polyelectrolyte complex micelles
Kuo, C., Leon, L., Chung, E. J., Huang, R., Sontag, T. J., Reardon, C. A., Getz, G. S., Tirrell, M., & Fang, Y. H. (2014) · Journal of Materials Chemistry B · doi:10.1039/c4tb00977k · Cited by 110
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“Several biomarkers of oxidation potential have been put forth, by measuring the formation of biologically active oxidized phospholipids, by the determination of endothelial superoxide production and NADPH oxidase, or by the measurement of paraoxonase activity [73].”
Small Things Matter: Relevance of MicroRNAs in Cardiovascular Disease
Peters, L. J. F., Biessen, E. A. L., Hohl, M., Weber, C., van der Vorst, E. P. C., & Santovito, D. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00793 · Cited by 101
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“However, further analysis revealed an increase in hepatic expression of AMPKα (encoded by PRKAA1), which is a negative regulator of the SREBP-1 pathway and also a direct target of miR-33.”
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Nakao, T., Horie, T., Baba, O., Nishiga, M., Nishino, T., Izuhara, M., Kuwabara, Y., Nishi, H., Usami, S., Nakazeki, F., et al. (2017) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.117.309768 · Cited by 81
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Baselga‐Escudero, L., Arola‐Arnal, A., Pascual‐Serrano, A., Ribas‐Latre, A., Casanova, E., Salvadó, M. J., Arola, L., & Bladé, C. (2013) · PLoS ONE · doi:10.1371/journal.pone.0069817 · Cited by 79
“Furthermore, the silencing of miR33 by knockout or antisense techniques in mice results in an improvement in the plasma lipid profile, increasing plasma high density lipoprotein-cholesterol (HDL-C) levels [15,17,18].”
BackgroundGiles, D. A., Ramkhelawon, B., Donelan, E. M., Stankiewicz, T. E., Hutchison, S. B., Mukherjee, R., Cappelletti, M., Karns, R. A., Karp, C. L., Moore, K. J., et al. (2016) · Molecular Metabolism · doi:10.1016/j.molmet.2016.09.008 · Cited by 81
“Oil Red O and CD68 staining were performed to detect neutral lipid and lesional macrophages as described previously [21].”
MethodSelf-citationMechanisms of MicroRNAs in Atherosclerosis
Schober, A., & Weber, C. (2016) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-012615-044135 · Cited by 78
RNA Therapeutics in Cardiovascular Precision Medicine
Laina, A., Gatsiou, A., Georgiopoulos, G. A., Stamatelopoulos, K. S., & Stellos, K. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00953 · Cited by 90
“Several experimental studies are investigating the use of miRNAs as therapeutic targets in atherosclerosis, coronary artery disease and myocardial infarction and clinical trials in humans are expected to test microRNAs either as antagomiRs or microRNA mimics in cardiovascular disease (Obad et al., 2011; Rayner et al.,…”
BackgroundOxidative stress in atherosclerosis: The role of microRNAs in arterial remodeling
Zampetaki, A., Dudek, K., & Mayr, M. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.06.025 · Cited by 79
“These mice show increased levels of circulating HDL, enhanced reverse cholesterol transport, and regression of established atherosclerotic plaques [68,69].”
MicroRNAs and Cardiovascular Disease Risk
Searles, C. D. (2024) · Current Cardiology Reports · doi:10.1007/s11886-023-02014-1 · Cited by 92
“Other liver-enriched miRNAs have been linked to the development of atherosclerosis through regulation of the LDL receptor (miR-148a, miR-128–1) [78, 79] and HDL levels (miR-33) [80].”
BackgroundLu, H. S., & Daugherty, A. (2015) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.115.305380 · Cited by 170
Epigenetic associations in relation to cardiovascular prevention and therapeutics
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“Among these are cardiac miRNAs, which, as studies indicate, can potentially be modulated by oligonucleotide-based therapies (Table 1) [10, 13, 107, 156, 159–181].”
BackgroundTargeted Suppression of miRNA-33 Using pHLIP Improves Atherosclerosis Regression
Zhang, X., Rotllan, N., Canfrán-Duque, A., Sun, J., Toczek, J., Moshnikova, A., Malik, S., Price, N. L., Araldi, E., Zhong, W., et al. (2022) · Circulation Research · doi:10.1161/circresaha.121.320296 · Cited by 75
Nonhuman Primates and Translational Research—Cardiovascular Disease
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“MiRNAs have been implicated in a plethora of biological pathways, including cholesterol metabolism, and contribute to the progression of a number of diseases (Rayner et al. 2011; Sun et al. 2014).”
BackgroundMetabolic reprogramming & inflammation: Fuelling the host response to pathogens
Gleeson, L. E., & Sheedy, F. J. (2016) · Seminars in Immunology · doi:10.1016/j.smim.2016.10.007 · Cited by 78
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“To generate CF-specific KO mice, we used a Pn-Cre line, which express Cre recombinase only in a subset of fibroblasts in the heart, and there is still no truly specific marker of CFs. Finally, inhibition of miR-33 is considered to be a potent therapeutic strategy for atherosclerosis because miR-33 has atherogenic effe…”
BackgroundInfluentialMa, Z., Deng, C., Hu, W., Zhou, J., Fan, C., Di, S., Liu, D., Yang, Y., & Wang, D. (2017) · Current Issues in Molecular Biology · doi:10.21775/cimb.022.041 · Cited by 70
“In addition, other miRNAs, including miR-33 (Rayner et al., 2011), miR-785 (Ramirez et al., 2011), miR-106b and miR-26 (Kim et al., 2012; Sun et al., 2012), have also been shown to regulate the expression of ABCA1, and whether there are interactions between LXRs and these miRNAs remains to be…”
BackgroundCholesterol homeostasis: Researching a dialogue between the brain and peripheral tissues
Gliozzi, M., Musolino, V., Bosco, F., Scicchitano, M., Scarano, F., Nucera, S., Zito, M. C., Ruga, S., Carresi, C., Macrì, R., et al. (2020) · Pharmacological Research · doi:10.1016/j.phrs.2020.105215 · Cited by 96
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High-Density Lipoproteins and Apolipoprotein A1.
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Vega‐Badillo, J., Gutiérrez‐Vidal, R., Hernández‐Pérez, H. A., Villamil‐Ramírez, H., León‐Mimila, P., Sánchez‐Muñoz, F., Morán‐Ramos, S., Larrieta‐Carrasco, E., Fernández‐Silva, I., Méndez‐Sánchez, N., et al. (2016) · Liver International · doi:10.1111/liv.13109 · Cited by 75
All’s well that transcribes well: Non-coding RNAs and post-stroke brain damage
Vemuganti, R. (2013) · Neurochemistry International · doi:10.1016/j.neuint.2013.07.014 · Cited by 71
“…Author M anuscript miR-33 which is located within the SREBF2 gene, suppresses expression of the cholesterol transporter ABC transporter A1 leading to lowered HDL levels and treatment with antimiR-33 has been shown to regress atherosclerosis in mice deficient in LDL receptors (Rayner et al., 2011).”
BackgroundJiang, H., Zhang, J., Du, Y., Jia, X., Yang, F., Si, S., Wang, L., & Hong, B. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.10.026 · Cited by 70
Potential therapeutic role of microRNAs in ischemic heart disease
Caroli, A., Cardillo, M. T., Galea, R., & Biasucci, L. M. (2013) · Journal of Cardiology · doi:10.1016/j.jjcc.2013.01.012 · Cited by 72
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Vertebrate and Invertebrate Respiratory Proteins, Lipoproteins and other Body Fluid Proteins
Hoeger, U., & Harris, J. (2020) · Subcellular Biochemistry · doi:10.1007/978-3-030-41769-7 · Cited by 67
Lai, L., Azzam, K. M., Lin, W.-C., Rai, P., Lowe, J. M., Gabor, K. A., Madenspacher, J. H., Aloor, J. J., Parks, J. S., Näär, A. M., et al. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.723056 · Cited by 67
HDL abnormalities in familial hypercholesterolemia: Focus on biological functions
Ganjali, S., Momtazi‐Borojeni, A. A., Banach, M., Kovanen, P. T., Stein, E. A., & Sahebkar, A. (2017) · Progress in Lipid Research · doi:10.1016/j.plipres.2017.05.001 · Cited by 68
mi RNA s, polyphenols, and chronic disease
Bladé, C., Baselga‐Escudero, L., Salvadó, M. J., & Arola‐Arnal, A. (2012) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201200454 · Cited by 64
Karunakaran, D., Richards, L., Geoffrion, M., Barrette, D., Gotfrit, R. J., Harper, M., & Rayner, K. J. (2015) · Arteriosclerosis, Thrombosis and Vascular Biology · doi:10.1161/atvbaha.115.306404 · Cited by 65
“We used an established dosing regimen of 10 mg/kg anti-miRNA oligonucleotides that maximize mature miRNA inhibition while limiting toxicity, ultimately resulting in the effective derepression of miR-33 targets in mouse models.(10,12) C57BL6/J mice were fed a HFD in conjunction with anti-miR treatment (10 mg/kg of cont…”
BackgroundMethodSelf-citationMicroRNA modulation of lipid metabolism and oxidative stress in cardiometabolic diseases
Aranda, J. F., Madrigal‐Matute, J., Rotllán, N., & Fernandez-Hernando, C. F. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.07.014 · Cited by 67
“In the first study, Rayner and colleagues [19] demonstrated that 2′-O-methoxyethyl (2′F/MOE)-modified anti-miR33 therapy enhances the regression of atherosclerosis in Ldlr / mice by increasing circulating HDL-cholesterol levels and RCT.”
MicroRNAs and atherosclerosis: New actors for an old movie
Santovito, D., Mezzetti, A., & Cipollone, F. (2012) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2012.03.007 · Cited by 64
“Inhibition of miR-33a produces atherosclerosis regression in mice and highlights the potential therapeutic use of this approach [58].”
BackgroundmiR-223 Exerts Translational Control of Proatherogenic Genes in Macrophages
Nguyen, M.-A., Hoang, H.-D., Rasheed, A., Duchez, A.-C., Wyatt, H., Cottee, M. L., Graber, T. E., Susser, L., Robichaud, S., Berber, İ., et al. (2022) · Circulation Research · doi:10.1161/circresaha.121.319120 · Cited by 74
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“Despite this, miR-1 has also been implicated in the modulation of a wide variety of Ca2+ handling proteins [87] and has been linked to ventricular arrhythmias [65].”
BackgroundRegression of Atherosclerosis: Insights from Animal and Clinical Studies
Feig, J. E. (2014) · Annals of Global Health · doi:10.1016/j.aogh.2013.12.001 · Cited by 71
MicroRNA regulation of lipid metabolism
Flowers, E., Froelicher, E. S., & Aouizerat, B. E. (2012) · Metabolism · doi:10.1016/j.metabol.2012.04.009 · Cited by 59
“[26] The same macrophages displayed changes in expression of inflammatory genes.”
BackgroundSenatus, L. M., López‐Díez, R., Egaña-Gorroño, L., Liu, J., Hu, J., Daffu, G. K., Li, Q., Rahman, K., Vengrenyuk, Y., Barrett, T. J., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.137289 · Cited by 70
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Eyeballing cholesterol efflux and macrophage function in disease pathogenesis
Sène, A., & Apte, R. S. (2013) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2013.10.007 · Cited by 56
Atherosclerosis: Insights into Vascular Pathobiology and Outlook to Novel Treatments
Wolf, M., & Hunziker, P. (2020) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-020-09961-y · Cited by 74
“ABCA1 expression is inhibited by miR-33, which offers the added value of delivering anti-miR-33 to macrophages, thereby neutralizing the inhibitory effect of miR-33, which was demonstrated in a non-targeted way [157].”
BackgroundMicroRNAs as Therapeutic Targets and Clinical Biomarkers in Atherosclerosis
Solly, E. L., Dimasi, C. G., Bursill, C. A., Psaltis, P. J., & Tan, J. T. M. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8122199 · Cited by 68
“Inhibition of miR-33a/b enhanced cholesterol efflux and regression of atherosclerotic plaques in Ldlr−/−mice [24] and improved lipid profiles in non-human primates [25,26].”
BackgroundFoks, A. C., van Puijvelde, G. H. M., Bot, I., ter Borg, M. N. D., Habets, K. L. L., Johnson, J. L., Yagita∥, H., van Berkel, T. J. C., & Kuiper, J. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1200708 · Cited by 60
“Experimental therapies aimed at achieving regression of atherosclerotic lesions in both human and animal models currently focus on lowering plasma LDL levels using statins (2) and improving reverse lipid transport and plasma high-density lipoprotein levels using agents such as phosphatidylcholine liposomes (28), CETP…”
BackgroundLipids, blood pressure and kidney update 2015
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The role of miRNAs in cardiovascular disease risk factors
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“played reduction in atherosclerosis progression [96] while antimiR-33a administration promoted atherosclerotic plaque regression in Ldlr / mice [93].”
Targeting smooth muscle microRNAs for therapeutic benefit in vascular disease
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“These miRNAs affect cholesterol metabolism (15-17), glucose homeostasis (18, 19), macrophage regulation (20,”
Complexity of microRNA function and the role of isomiRs in lipid homeostasis
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Epigenetic regulation of cholesterol homeostasis
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“Subsequent studies of hypercholesterolemic men treated with kale juice (also rich in sulforaphane) in demonstrated similar beneficial increases in HDL-cholesterol and a significant and clinically relevant decrease in the atherogenic index (Kim et al., 2008).”
BackgroundInfluentialSchmidt, U., Herrmann, L., Hagl, K., Novak, B., Huber, C. W., Holsboer, F., Wotjak, C. T., & Buell, D. R. (2013) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2013.00066 · Cited by 62
“MiR33 was found to be downregulated in the hippocampus of rats with status epilepticus (60), to regulate the cell cycle (61, 62), to be associated with mouse atherosclerosis (63, 64), as well as with metabolism of cholesterol (65, 66).”
Background
Metadata
- Authors
- Rayner, K. J., Sheedy, F. J., Esau, C. C., Hussain, F. N., Temel, R. E., Parathath, S., van Gils, J. M., Rayner, A. J., Chang, A. N., Suarez, Y., Fernandez-Hernando, C., Fisher, E. A., & Moore, K. J.
- Affiliations
- New York University (US)
- Regulus Therapeutics (United States) (US)
- Wake Forest University Health Sciences (US)
- Corresponding author
- Moore, Kathryn J.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2011-07-01
- Volume
- 121
- Issue
- 7
- Pages
- 2921-2931
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3223840
- OpenAlex
- W2168964544
- Cited by
- 690
- References
- 0
- Citations by year
- 2026: 14 · 2025: 27 · 2024: 21 · 2023: 35 · 2022: 41 · 2021: 36 · 2020: 38 · 2019: 43 · 2018: 45 · 2017: 48 · 2016: 63 · 2015: 62 · 2014: 82 · 2013: 71 · 2012: 50
- FWCI
- 70.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Funders
- National Institutes of Health (5r00hl088528-05)
- Canadian Institutes of Health Research
- National Institute on Aging (R01AG020255)
- National Heart, Lung, and Blood Institute (R01HL084312, R00-HL088528, K99HL088528, P01HL098055, R01HL108182, R01HL107953)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- miR-33, reverse cholesterol transport, HDL cholesterol, atherosclerosis regression, ABCA1, SREBF2, LDL receptor-deficient mice, atherosclerotic plaque, plaque macrophages, cholesterol efflux, plaque stability, inflammation
- MeSH terms
- Animals, Humans, Cholesterol, HDL, Liver, Macrophages, Mice, Inbred C57BL, Random Allocation, Receptors, LDL, Gene Expression, Mice, Knockout, ATP-Binding Cassette Transporters, MicroRNAs, Atherosclerosis, Lipid Metabolism, Mice, ATP Binding Cassette Transporter 1
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