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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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“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]
In the citing paper
“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]
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Cites
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Items 401–500 of 642
The power of microRNA regulation—insights into immunity and metabolism
Oliveto, S., Manfrini, N., & Biffo, S. (2025) · FEBS Letters · doi:10.1002/1873-3468.70039 · Cited by 21
“Moreover, miR-33 inhibition promotes reverse cholesterol transport and regression of atherosclerotic plaques in mouse models of atherosclerosis [89].”
Cardiac Metabolism and MiRNA Interference
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Decoding microRNA drivers in atherosclerosis
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Cardiovascular inflammation: RNA takes the lead
Martens, C. R., Bansal, S. S., & Accornero, F. (2019) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2019.03.012 · Cited by 23
“This could be one mechanism by which HDL protects the vasculature from atherosclerosis.”
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Novel Role of miR-33 in Regulating of Mitochondrial Function
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Thirunavukkarasu, S., de Silva, K., Plain, K. M., & Whittington, R. J. (2014) · Critical Reviews in Microbiology · doi:10.3109/1040841x.2014.932327 · Cited by 15
“…inhibiting this could alleviate certain pathological conditions associated with altered lipid metabolism such as atherosclerosis (Najafi- Shoushtari et al., 2010; Rayner et al., 2010, 2011) and a recently published study by Meng et al. (2014) reported miRNAs associated with latent tuberculosis.”
BackgroundHepatic ABCA1 Expression Improves β-Cell Function and Glucose Tolerance
de Haan, W., Karasinska, J. M., Ruddle, P., & Hayden, M. R. (2014) · Diabetes · doi:10.2337/db14-0548 · Cited by 20
“HDL raising therapies are currently under development for the treatment of patients with dyslipidemia (23-25).”
BackgroundMicroRNA-Management of Lipoprotein Homeostasis
Sun, X., & Feinberg, M. W. (2014) · Circulation Research · doi:10.1161/circresaha.114.304228 · Cited by 19
“Given that miR-33 inhibition has been extensively studied from rodents to nonhuman primates, the findings from Allen et al(20) also beg the larger question—how do we still reconcile their observations from the other miR-33 inhibition studies, in which no inductive effects on triglyceride or VLDL-triglyceride were obse…”
BackgroundResultA big role for small RNAs in HDL homeostasis
Ouimet, M. I., & Moore, K. J. (2013) · Journal of Lipid Research · doi:10.1194/jlr.r036327 · Cited by 21
Self-citationMicroRNAs as a Potential Biomarker in the Diagnosis of Cardiovascular Diseases
Kramna, D., Riedlová, P., & Jiřík, V. (2023) · Medicina · doi:10.3390/medicina59071329 · Cited by 19
“Experimental studies have obtained interesting results that blocking miR-148a increased the clearance of LDL particles in liver tissue [32] and blockade of miR-33 increased HDL levels by up to 50% while reducing atherosclerotic plaques [34].”
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New insights into macrophage subsets in atherosclerosis
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“3 In vivo analysis of reverse cholesterol transport As noted above, anti-miR-33 treatment of LDLr-/- mice led to increased reverse cholesterol transport (RCT) and the regression of atherosclerosis [34].”
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“Some miRNA-based therapies have already been proposed for the treatment of obesity comorbidities, such as antisense miR-122 therapy for NAFLD [120] and antisense miR-33 for atherosclerosis [121,122], although none of them specifically intend to reduce OS.”
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MicroRNA-33 suppresses CCL2 expression in chondrocytes
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Uncomplicating the Macrovascular Complications of Diabetes: The 2014 Edwin Bierman Award Lecture
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“In addition, anti–miR-33 treatment resulted in elevated HDL levels in diabetic mice, concomitant with increased hepatic expression of ABCA1, consistent with previous studies (75).”
ResultAnti-atherosclerosis or No Anti-atherosclerosis
Näär, A. M. (2013) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.112.301021 · Cited by 17
“Indeed, in marked contrast to the Marquart et al12 study in this issue, the recent nonhuman primate study of Rayner et al,11 which is also longitudinal, did show a sustained elevation of HDL-C over 12 weeks in response to miR-33a/b antisense antagonism, as well as a strong decrease in triglycerides.”
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“mediated by ABCA1, enhances mitochondrial function, and changes the polarization of macrophages.(158) Anti-miR33 therapy de-repressed genes (PGC-1α, pyruvate dehydrogenase kinase 4 (PDK4), and solute”
BackgroundThe Role of MicroRNAs in Hyperlipidemia: From Pathogenesis to Therapeutical Application
Xiang, Y., Li, M., Zuo, M., Song, G., Tan, L.-M., & Yang, Z. (2022) · Mediators of Inflammation · doi:10.1155/2022/3101900 · Cited by 24
“This suggested that miR-33a is an important regulator of macrophage cholesterol efflux and HDL biogenesis and is a promising target for treatment of atherosclerosis [86, 87].”
BackgroundXu, Y., Murphy, A. J., & Fleetwood, A. J. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23042234 · Cited by 23
“MicroRNA 33 (miR33) is a transcriptional repressor of ABCA1 and ABCG1 in diabetes-associated hyperglycemic environments [74,78].”
BackgroundKowara, M., Borodzicz-Jażdżyk, S., Rybak, K., Kubik, M., & Cudnoch‐Jędrzejewska, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115718 · Cited by 17
Han, R., Luo, J., Wang, L., Li, L., & Zheng, H. (2021) · Cardiovascular Toxicology · doi:10.1007/s12012-021-09663-0 · Cited by 17
“Antagonism of miR-33 in mice promotes reverse cholesterol transport and regression of atherosclerosis [27].”
BackgroundPagano, S., Magenta, A., D'Agostino, M., Martino, F., Barillà, F., Satta, N., Frias, M. A., Ronca, A., Mach, F., Gencer, B., et al. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8122035 · Cited by 22
“While previous studies suggested that miR-33 may represent therapeutic target for the treatment of cardiovascular disease [24,25], a recent work showed that miR-33 deletion in mice results in dyslipidemia, obesity, and insulin resistance [26], assigning a role for miR-33 that is much more complex than what has been co…”
ResultHarnessing the Therapeutic Potential of MicroRNAs for Cardiovascular Disease
Calway, T., & Kim, G. H. (2014) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/1074248414552902 · Cited by 17
“ABCA1 is a protein transporter involved in cholesterol efflux, so lower levels result in higher plasma HDL levels,(98) which has been observed both in mouse and nonhuman primate study with antagomirs.(55,56) In another study, the progression of atherosclerosis measured by plaque size and macrophage content was slowed…”
ResultRegulatory T cells and macrophages in atherosclerosis: from mechanisms to clinical significance
Ouyang, X., & Liu, Z. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1435021 · Cited by 20
“It was previously recognized that microRNA-33 (miR-33) and its host genes cooperated to regulate cholesterol homeostasis (86, 87) and reduce atherosclerotic plaque size (88, 89).”
Esobi, I. C., Oladosu, O., Echesabal-Chen, J., Powell, R. R., Bruce, T. F., & Stamatikos, A. (2023) · Journal of Lipids · doi:10.1155/2023/8241899 · Cited by 19
“However, what does appear to be established is that ablating miR-33a in monocytes/macrophages exhibits atheroprotective effects via increasing ABCA1-dependent cholesterol efflux [35, 36].”
BackgroundThe influence of epigenetics and inflammation on cardiometabolic risks
Raghubeer, S. (2023) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2023.02.006 · Cited by 23
Howe, K. L., Cybulsky, M. I., & Fish, J. E. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.888390 · Cited by 16
“One heavily studied target is microRNA-33 (110, 111).”
BackgroundTao, Y., Xu, S., Wang, J., Xu, L., Zhang, C., Chen, K., Lian, Z., Zhou, J., Xie, H., Zheng, S., et al. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00921 · Cited by 20
Small Molecules with Big Impacts on Cardiovascular Diseases
Azad, F. M., Arabian, M., Maleki, M., & Malakootian, M. (2020) · Biochemical Genetics · doi:10.1007/s10528-020-09948-z · Cited by 21
Song, M., Xu, S., Zhong, A., & Zhang, J. (2019) · Clinical Immunology · doi:10.1016/j.clim.2019.03.001 · Cited by 18
Dlouhá, D., Bláha, M., Bláha, V., Fátorová, I., Hubáček, J., Stávek, P., Lánská, V., Parikova, A., & Piťha, J. (2017) · Atherosclerosis Supplements · doi:10.1016/j.atherosclerosissup.2017.05.037 · Cited by 16
Emerging Role of MicroRNAs in the Regulation of Lipid Metabolism
Fernandez-Hernando, C. F. (2012) · Hepatology · doi:10.1002/hep.25960 · Cited by 16
“As expected by the significant increase in HDL levels observed in mice treated with anti-miR-33 oligonucleotides, the inhibition of miR-33 expression promotes reverse cholesterol transport and regression of atherosclerosis.(15) Overexpression of miR-33 also represses genes involved in the regulation of fatty acid oxid…”
Circulating miRNA profiling to identify biomarkers of dysmetabolism.
Tomaselli, S., Panera, N., Gallo, A., & Alisi, A. (2012) · Biomarkers in Medicine · doi:10.2217/bmm.12.91 · Cited by 16
MicroRNA in pulmonary vascular disease.
Rothman, A., Chico, T., & Lawrie, A. (2014) · Progress in Molecular Biology and Translational Science · doi:10.1016/b978-0-12-386930-2.00003-3 · Cited by 16
Salama, R. M., Eissa, N., Doghish, A. S., Abulsoud, A. I., Abdelmaksoud, N. M., Mohammed, O. A., Mageed, S. S. A., & Darwish, S. F. (2024) · Frontiers in Aging · doi:10.3389/fragi.2024.1373741 · Cited by 18
Ishida, N., Yamada, H., & Hirose, M. (2021) · Nutrients · doi:10.3390/nu13113765 · Cited by 15
“[48] showed that the elevated ABCA1 expression increased plasma HDL cholesterol in LDLR-KO mice.”
BackgroundMicroRNAs and Long Noncoding RNAs in Coronary Artery Disease
Zaręba, Ł., Fitas, A., Wolska, M., Junger, E., Eyileten, C., Wicik, Z., Rosa, S. D., Siller-Matula, J. M., & Postula, M. A. (2020) · Cardiology Clinics · doi:10.1016/j.ccl.2020.07.005 · Cited by 14
Genetically Encoded Reporter Genes for MicroRNA Imaging in Living Cells and Animals
Song, Y., Xu, Z., & Wang, F. (2020) · Molecular Therapy: Nucleic Acids · doi:10.1016/j.omtn.2020.06.021 · Cited by 15
Foroutan, T., Farhadi, A., Abroun, S., & Soltani, B. (2017) · Cell journal · doi:10.22074/cellj.2018.4393 · Cited by 15
“It is well known that p53 upregulates miR-145 expression (12).”
BackgroundCoffey, A. R., Smallwood, T., Albright, J., Hua, K., Kanke, M., Pomp, D., Bennett, B. J., & Sethupathy, P. (2017) · Physiological Genomics · doi:10.1152/physiolgenomics.00050.2017 · Cited by 18
“Several hepatic miRNAs have been associated with atherosclerosis and hyperlipidemia, including microRNA (miR)-27 (44, 49), miR-122 (11), miR-148a (15), miR-33 (18, 39, 40), and miR-30c (47).”
BackgroundDevelopment of Antisense Drugs for Dyslipidemia
Yamamoto, T., Wada, F., & Harada‐Shiba, M. (2016) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv16001 · Cited by 17
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“In another example, chemically modified oligonucleotides were used for an inhibition of miR33a/b [22].”
MethodInterfering Nanoparticles for Silencing MicroRNAs
Baigude, H., & Rana, T. M. (2012) · Methods in enzymology on CD-ROM/Methods in enzymology · doi:10.1016/b978-0-12-391858-1.00017-4 · Cited by 17
“Chemically stabilized anti-miR sequences with 2′-fluoro and/or methoxyethyl groups have increased inhibitory activities (Rayner et al., 2011).”
Vladimirov, S. S., Tomasevic, M., Popov, N., Munjas, J., de Gonzalo‐Calvo, D., & Sopić, M. (2025) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2025.06.005 · Cited by 14
Inhibition of microRNA-33b in humanized mice ameliorates nonalcoholic steatohepatitis
Miyagawa, S., Horie, T., Nishino, T., Koyama, S., Watanabe, T., Baba, O., Yamasaki, T., Sowa, N., Otani, C., Matsushita, K., et al. (2023) · Life Science Alliance · doi:10.26508/lsa.202301902 · Cited by 14
“The inhibition of miR-33a/b has been shown to improve HDL biosynthesis in the liver and increase blood HDL-C levels in nonhuman primates (Rayner et al, 2011a).”
Recent Advances on the Role and Therapeutic Potential of Regulatory T Cells in Atherosclerosis
Tanaka, T., Sasaki, N., & Rikitake, Y. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10245907 · Cited by 18
Santos, D., & Carvalho, E. (2021) · The Journal of Physiology · doi:10.1113/jp280917 · Cited by 17
“Moreover, targeted inhibition for miR-33 has been considered as a therapeutic approach for the treatment of cardiometabolic diseases in obese mice and non-human primate models (Rayner et al. 2011a; Rottiers et al. 2013).”
BackgroundInfluentialComparative microRNA Transcriptomes in Domestic Goats Reveal Acclimatization to High Altitude
Feng, S., Ma, J., Long, K., Zhang, J., Qiu, W., Li, Y., Jin, L. G., Wang, X., Jiang, A., Liu, L., et al. (2020) · Frontiers in Genetics · doi:10.3389/fgene.2020.00809 · Cited by 16
miR-33 regulation of adaptive fibrotic response in cardiac remodeling
Zhang, X.-B., & Fernández-Hernando, C. (2017) · Circulation Research · doi:10.1161/circresaha.117.310575 · Cited by 14
“miR-33 inhibition is considered to be an effective therapeutic strategy for treating atherosclerosis in the mice.(12,13) To promote protective effects on macrophage cholesterol homeostasis and to avoid adverse effects on cardiac dysfunction, effective strategies such as cell- or tissue-specific targeting of miR-33 may…”
Huang, C., & Zhang, Y. (2013) · Current Pharmaceutical Biotechnology · doi:10.2174/138920101131400228 · Cited by 14
“Nevertheless, miRNA antagonists might be a possible target for the treatment of cardiovascular and metabolic disorders [60, 61].”
BackgroundThe Plaque “Micro” Environment: microRNAs Control the Risk and the Development of Atherosclerosis
Rayner, K. J., & Moore, K. J. (2012) · Current Atherosclerosis Reports · doi:10.1007/s11883-012-0272-x · Cited by 14
Self-citationPhysiological and Pathological Functions of Mammalian MicroRNAs
Liu, M., Jiang, S., Lu, Z., Li, Y., & Young, K. H. (2010) · Elsevier eBooks · doi:10.1016/b978-0-08-046884-6.00223-2 · Cited by 10
Is microRNA-33 an Appropriate Target in the Treatment of Atherosclerosis?
Sidorkiewicz, M. (2023) · Nutrients · doi:10.3390/nu15040902 · Cited by 16
“The results of many studies demonstrate that silencing of miR-33 in mice, with a variety of methods like targeted deletion [17], anti-sense nucleotides [18,19] or viral delivery inhibitors [21,38], significantly increased ABCA1 expression and the level of HDL in blood.”
BackgroundResultJiang, Y., Yang, Z.-G., Wang, J., Shi, R., Han, P., Qian, W., Yan, W., & Li, Y. (2022) · Cardiovascular Diabetology · doi:10.1186/s12933-022-01700-8 · Cited by 17
“Treatment to raise HDL-C levels regressed coronary plaque and reduced lipid content in plaque [30].”
BackgroundmicroRNAs involved in psoriasis and cardiovascular diseases
Sileno, S., Beji, S., D'Agostino, M., Carassiti, A., Melillo, G., & Magenta, A. (2021) · Vascular Biology · doi:10.1530/vb-21-0007 · Cited by 17
Prakhar, P., Bhatt, B., Lohia, G. K., Shah, A., Mukherjee, T., Kolthur‐Seetharam, U., Sundaresan, N. R., Rajmani, R. S., & Balaji, K. N. (2023) · PLoS Pathogens · doi:10.1371/journal.ppat.1011731 · Cited by 12
“Existing literature suggests that genes responsible for cholesterol biosynthesis and homeostasis are epigenetically governed by miRNAs (miR-33a, miR-185), histone deacetylases (HDAC3, SIRT2, SIRT6) and HMTs (G9a) under distinct conditions [22] [23].”
Worthmann, A., Schlein, C., Berbée, J. F. P., Rensen, P. C. N., Heeren, J., & Bartelt, A. (2019) · Nutrients · doi:10.3390/nu11020463 · Cited by 18
Ma, F., Li, T., Zhang, H.-J., & Wu, G.-J. (2016) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000419 · Cited by 13
“MiR-155 and miR-146a may participate in the inflammatory response in As lesions by regulating the TLR signaling pathway, and play an important role in the process of Th differentiation(14); miR-29 increased As lesions by promoting Vascular Smooth Muscle Cell migration and inflammatory responses(15); miR-33 participate…”
BackgroundMicroRNAs in diagnosis and therapeutics
Atri, C., Guerfali, F. Z., & Laouini, D. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-815669-8.00006-3 · Cited by 25
Fuentevilla-Álvarez, G., Soto, M. E., Robles-Herrera, G. J., Vargas-Alarcón, G., Sámano, R., Meza-Toledo, S., Huesca-Gómez, C., & Gamboa, R. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25137078 · Cited by 12
Very low HDL levels: clinical assessment and management
Bonilha, I., Luchiari, B., Nadruz, W., & Sposito, A. (2023) · Archives of Endocrinology and Metabolism · doi:10.20945/2359-3997000000585 · Cited by 12
Sung, H., Choi, E., Han, J., Yun, J.-C., Im, S.-W., Kim, H.-S., Park, E.-M., & Ahn, J.-H. (2021) · Scientific Reports · doi:10.1038/s41598-021-91982-x · Cited by 12
Semo, J., Chernin, G., Jonas, M., Shimoni, S., & George, J. (2019) · Lipids in Health and Disease · doi:10.1186/s12944-019-1155-8 · Cited by 12
Metabolic adaptation of macrophages in chronic diseases
Conza, G. D., & Ho, P. (2017) · Cancer Letters · doi:10.1016/j.canlet.2017.11.023 · Cited by 12
Avitabile, C., Cimmino, A., & Romanelli, A. (2014) · Journal of Medicinal Chemistry · doi:10.1021/jm5006594 · Cited by 14
Wang, Z., Guo, D., Yang, B., Wang, J., Wang, R., Wang, X.-W., & Zhang, Q.-Y. (2014) · PLoS ONE · doi:10.1371/journal.pone.0110288 · Cited by 12
High Density Lipoproteins Put Out the Fire
Moore, K., & Fisher, E. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.01.009 · Cited by 12
“…increase in functional HDL particles has been reported to reduce the expression in plaque macrophages of inflammatory mediators, an effect similar to that in De Nardo et al., but also to increase the expression of markers of the anti-inflammatory M2 state (Feig et al., 2011; Rayner et al., 2011).”
ResultSelf-citationWang, J., Zhou, J., Zheng, Q., Gan, H., & Wang, H. (2014) · Therapeutic Apheresis and Dialysis · doi:10.1111/1744-9987.12040 · Cited by 11
Soh, J., & Hussain, M. M. (2013) · Nutrition & Metabolism · doi:10.1186/1743-7075-10-56 · Cited by 11
“plasma HDL concentrations [10,11].”
Liu, J., Liu, X.-Q., Liu, Y., Sun, Y.-N., Li, S., Li, C.-M., Li, J., Tian, W., Shang, X.-M., & Zhou, Y.-T. (2016) · Molecular Medicine Reports · doi:10.3892/mmr.2015.4563 · Cited by 12
“The use of anti-miRs against ABCA1-associated miRs, such as miR-33 and miR-144, have been confirmed to be potentially therapeutic in the attenuation of the atherosclerotic progress in murine models of atherosclerosis (25,27).”
Lipid metabolic alterations in cancer: Common pathophysiology with cardiovascular disease
Llena-Meler, M., Canfrán‐Duque, A., Madrigal‐Matute, J., & Rotllán, N. (2026) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2026.01.003 · Cited by 12
Li, X., Hernandez, R., Zhang, X., Tang, S., Yuan, X., Wu, J., Pham, K., Rawal, H. C., Heinrich, E. C., Zhang, S., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-67387-z · Cited by 10
“For sncRNAs, miRNA-33 coordinates with Srebp host genes to regulate cholesterol homeostasis in both mice and non-human primates 8 – 10 . miRNA-148a targets both Ldlr and Abca1 to affect LDL and HDL levels in mice 4,12 . miRNA-30c and miRNA-483 can also reduce hyperlipidemia by targeting Mtp and…”
Endo, Y., Sasaki, K., & Ikewaki, K. (2024) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv22020 · Cited by 11
“Other studies have reported that miR-33 23) , Farnesoid X receptor (FXR) 24) , and low-density lipoprotein receptor-related protein 1 (LRP-1) 25) are involved in modulating RCT activity.”
BackgroundChen, D., Ji, Q., Liu, J., Cheng, F., Zheng, J., Ma, Y., He, Y., Zhang, J., & Song, T. (2023) · Biomolecules · doi:10.3390/biom13091344 · Cited by 15
“For example, extensive research has highlighted the functional involvement of miR-33 in cellular metabolism, particularly in the maintenance of cholesterol homeostasis [81,82].”
BackgroundRotllán, N., Zhang, X., Canfrán‐Duque, A., Goedeke, L., Griñán, R., Ramírez, C. M., Suárez, Y., & Fernandez-Hernando, C. F. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.113419 · Cited by 14
Studies in a Murine Granuloma Model of Instilled Carbon Nanotubes: Relevance to Sarcoidosis
Barna, B., Malur, A., & Thomassen, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22073705 · Cited by 11
“Mediators and Status Role in Pathophysiology Pulmonary Locations MWCNT MODEL S RCOIDOSIS Peroxisome proliferator-activated receptor gamma (PPARγ)—Defi- ciency Granuloma Formation [27] Bronchoalveolar lavage (BAL) cells [27] BAL cells [28] Lipid Dysregulation [22] Fibrosis [40] Inflammatory Profiles [26] Osteopontin—El…”
BackgroundInfluentialLncRNA-modulated autophagy in plaque cells: a new paradigm of gene regulation in atherosclerosis?
Ren, K., Xu, X., Yu, X.-H., Li, M., Shi, M., Liu, Q.-X., Jiang, T., Zheng, X., Yin, K., & Zhao, G.-J. (2020) · Aging · doi:10.18632/aging.103786 · Cited by 12
“In addition, miR-33 antagonism exerts antiatherogenic effects by promoting the ABCA1-mediated efflux of cholesterol from plaque macrophages [45].”
BackgroundMicroRNA-33 promotes the replicative senescence of mouse embryonic fibroblasts by suppressing CDK6
Xu, S., Huang, H., Li, N., Zhang, B., Jia, Y., Yang, Y.-K., Yuan, Y., Xiong, X., Wang, D., Zheng, H., et al. (2016) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2016.04.016 · Cited by 11
Epigenética en la arteriosclerosis
Guardiola, M., Vallvé, J.-C., Zaina, S., & Ribalta, J. (2015) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/j.arteri.2015.04.002 · Cited by 8
Unlocking the Door to New Therapies in Cardiovascular Disease: MicroRNAs Hold the Key
Nguyen, M.-A., Karunakaran, D., & Rayner, K. J. (2014) · Current Cardiology Reports · doi:10.1007/s11886-014-0539-7 · Cited by 12
Self-citationXuezhikang Therapy Increases miR-33 Expression in Patients with Low HDL-C Levels
Cao, R., Bai, Y., Sun, L., Zheng, J., Zu, M., Du, G., & Ye, P. (2014) · Disease Markers · doi:10.1155/2014/781780 · Cited by 12
Liu, C., Pan, X., Hao, Z., Wang, X., Wang, C., & Song, G. (2024) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2024.12615 · Cited by 11
“Although multiple animal experiments have confirmed that miR-33 is an important small RNA in regulating lipid metabolism, few studies have been conducted on its expression levels in circulating blood in individuals with hyper-lipidemia (20,58,63-67).”
BackgroundDlouhá, D., Bláha, M., Huckova, P., Lánská, V., Hubáček, J., & Bláha, V. (2023) · Genes · doi:10.3390/genes14081571 · Cited by 10
Exploring the Regulatory Role of ncRNA in NAFLD: A Particular Focus on PPARs
Mukherjee, A. G., Wanjari, U. R., Gopalakrishnan, A. V., Katturajan, R., Kannampuzha, S., Murali, R., Namachivayam, A., Ganesan, R., Renu, K., Dey, A., et al. (2022) · Cells · doi:10.3390/cells11243959 · Cited by 16
“Its blockage boosts reverse cholesterol transport, decreases LDL and TGs, and raises plasma HDH [98].”
BackgroundImpact of microRNA Regulated Macrophage Actions on Adipose Tissue Function in Obesity
Matz, A., Qu, L., Karlinsey, K. S., & Zhou, B. (2022) · Cells · doi:10.3390/cells11081336 · Cited by 11
“In particular, miR-33 targets ABCA1 in mouse and human cells to repress cholesterol efflux [61]; antimiR-33 treatment resulted in plaque regression via macrophage-mediated cholesterol removal [62].”
BackgroundLiver-specific microRNA-185 knockout promotes cholesterol dysregulation in mice
Chen, C., Matye, D. J., Wang, Y., & Li, T. (2020) · Liver Research · doi:10.1016/j.livres.2020.09.001 · Cited by 14
Saito, M., Ishida, N., Yamada, H., Ibi, M., & Hirose, M. (2020) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b20-00162 · Cited by 10
Non-coding RNAs in aneurysmal aortopathy
Spin, J. M., Li, D. Y., Mäegdefessel, L., & Tsao, P. S. (2018) · Vascular Pharmacology · doi:10.1016/j.vph.2018.06.008 · Cited by 13
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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