MicroRNA-33 and the SREBP Host Genes Cooperate to Control Cholesterol Homeostasis
Open accessAbstract
miR-33 in Cholesterol Control: With the well-established link between serum cholesterol levels and cardiovascular disease and the availability of effective cholesterol-lowering drugs, cholesterol screening has rapidly become a routine part of health care. Yet, much remains to be learned about how cholesterol levels are regulated at the cellular level (see the Perspective by Brown et al. ). Now, Najafi-Shoushtari et al. (p. 1566 , published online 13 May) and Rayner et al. (p. 1570 , published online 13 May) have discovered a new molecular player in cholesterol control—a small noncoding RNA that, intriguingly, is embedded within the genes coding for sterol regulatory element-binding proteins (SREBPs), transcription factors already known to regulate cholesterol levels. This microRNA, called miR-33, represses expression of the adenosine triphosphate–binding cassette transporter A1, a protein that regulates synthesis of high-density lipoprotein (HDL, or “good” cholesterol) and that helps to remove “bad” cholesterol from the blood. Reducing the levels of miR-33 in mice boosted serum HDL levels, suggesting that manipulation of this regulatory circuit might be therapeutically useful.
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Pharmacological inhibition of miR-33 increased plasma HDL cholesterol levels in mice and primates, leading to a marked reduction of atherosclerosis phenotypes.
“Pharmacological inhibition of miR-33 increased plasma high-density lipoprotein cholesterol levels in mice (Horie et al., 2010;Najafi-Shoushtari et al., 2010;Rayner et al., 2011a) and primates (Rayner et al., 2011b;Rottiers et al., 2013), leading to a marked reduction of atherosclerosis phenotypes.”
From microRNA-33 Regulates ApoE Lipidation and Amyloid-β Metabolism in the Brain (2015) · cites this paper as Najafi-Shoushtari et al., 2010
The Results report that antisense inhibition of miR-33 significantly increased plasma HDL cholesterol in mice. This paper does not report miR-33 inhibition in primates or demonstrate a reduction in atherosclerosis phenotypes; the citing sentence assigns the primate finding to other citations. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn vivo antagonism or genetic deletion of miR-33 enhances hepatic ABCA1 expression and increases circulating HDL-cholesterol.
“in vivo antagonism or genetic deletion of miR-33 enhances hepatic ABCA1 expression and increases circulating HDL-cholesterol (HDL-C) (Marquart et al., 2010; Najafi-Shoushtari et al., 2010; Rayner et al., 2010).”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Najafi-Shoushtari et al., 2010
The Results report that in vivo miR-33a antisense treatment significantly increased plasma HDL-cholesterol in mice. They describe only modest effects on hepatic ABCA1 mRNA and protein, rather than clearly establishing the claimed enhancement, and do not report genetic deletion of miR-33. (LLM, conf=0.88)
Experimental — accuracy not yet measuredDifferences in miRNA expression vary between cell types, suggesting that the role of miR-33b in the liver and other tissues may be considerably more important.
“These differences in miRNA expression vary between cell types suggesting that the role of miR-33b in the liver, where miR-33 is most highly expressed both in our mouse model and in human tissues (Najafi-Shoushtari et al., 2010), and other tissues may be considerably more important.”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Najafi-Shoushtari et al., 2010
The Results (page unavailable) report miR-33a/b expression across human and mouse tissues, but do not state that expression is highest in human liver—the specific point to which this citation is attached. The citing authors’ mouse-model observation and inference about miR-33b’s importance are their own, rather than findings attributed to this source. (LLM, conf=0.78)
Experimental — accuracy not yet measuredIn miR-33a knockout mice or when miR-33a is suppressed by synthetic nucleic acids such as antagomirs, the expression of ABCA1 in macrophages and the liver is increased.
“In miR-33a knockout mice or when miR-33a is suppressed by synthetic nucleic acids such as antagomirs, the expression of ABCA1 in macrophages and the liver is increased 11 - 15) .”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [11]
The Results (page unavailable) report that anti-miR-33a/b oligonucleotides increased ABCA1 in cell lines including mouse macrophages and human liver carcinoma cells. In mice given miR-33a antisense, the paper reports only modest effects on hepatic ABCA1; it does not report results from miR-33a knockout mice. Thus, it supports the antisense finding but not the full claim as stated. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMicroRNA-33 targets ABCA1 and ABCG1 in vivo.
“MicroRNA (miR)-33 is known to target ABCA1 and ABCG1 in vivo.”
From MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE <sup>−/−</sup> Mice (2012) · cites this paper as [17]
The Results show that miR-33 targets the ABCA1 3′UTR, and the mouse experiment reports an HDL increase consistent with miR-33a regulation of ABCA1-dependent cholesterol efflux in vivo. The passages do not show that miR-33 targets ABCG1 in vivo; a search for ABCG1 returned no passage addressing it. (LLM, conf=0.87)
Experimental — accuracy not yet measured
Two miR-33 genes are present in humans: miR-33b in intron 17 of Srebp-1 on chromosome 17, and miR-33a in intron 16 of Srebp-2 on chromosome 22.
“Two miR-33 genes are present in humans: miR-33b, which is present in intron 17 of the Srebp-1 gene on chromosome 17, and miR-33a, which is located in intron 16 of the Srebp-2 gene on chromosome 22.”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [13]
The Results identify two human miR-33 isoforms and place miR-33b in intron 17 of SREBP-1 on chromosome 17. They place miR-33a in intron 15 of SREBP-2 on chromosome 22, not intron 16 as the citing sentence states. (LLM, conf=0.95)
Experimental — accuracy not yet measuredDuring sterol-limited states, miR-33a is coincidentally generated with Srebp-2 transcription and works to increase cellular cholesterol levels by limiting cholesterol export through down-regulation of ABC transporters, ABCA1 and ABCG1.
“We and others have recently established that, during sterol-limited states, miR-33a is coincidentally generated with Srebp-2 transcription and works to increase cellular cholesterol levels by limiting cholesterol export through the down-regulation of ABC transporters, ABCA1 and ABCG1 (12–14).”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [13]
The Results report that cholesterol depletion increased both miR-33a and its SREBP-2 host gene in mouse macrophages, while reducing ABCA1 protein. They also show that miR-33a reduced cholesterol efflux and promoted intracellular cholesterol retention through ABCA1 repression. The passages do not support the additional claim that miR-33a down-regulates ABCG1. (LLM, conf=0.88)
Experimental — accuracy not yet measuredmiR-33a and miR-33b are intronic miRNAs encoded within the SREBP-2 and SREBP-1 genes respectively.
“miR-33a and miR-33b are intronic miRNAs encoded within the SREBP-2 and SREBP-1 genes respectively (Marquart et al., 2010; Najafi-Shoushtari et al., 2010; Rayner et al., 2010).”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Najafi-Shoushtari et al., 2010
miR-33a and miR-33b are co-transcribed along with SREBP-2 and SREBP-1 and work in concert with their host genes to help maintain proper lipid levels within the cell.
“This work led to the demonstration that miR-33a and miR-33b are co-transcribed along with SREBP-2 and SREBP-1, and work in concert with their host genes to help maintain proper lipid levels within the cell (Davalos et al., 2011; Marquart et al., 2010; Najafi-Shoushtari et al., 2010; Rayner et al., 2010).”
From Genetic dissection of the impact of miR-33a and miR-33b during the progression of atherosclerosis (2017) · cites this paper as Najafi-Shoushtari et al., 2010
The most well-known target gene of miR-33a/b is ABCA1.
“The most well-known target gene of miR-33a/b is ATP-binding cassette subfamily A member 1 (ABCA1).”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [11]
miR-33 controls cholesterol homeostasis based on knockdown experiments using antisense technology.
“Recent reports, including ours, have indicated that miR-33 controls cholesterol homeostasis based on knockdown experiments using antisense technology.16–18”
From MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE <sup>−/−</sup> Mice (2012) · cites this paper as [17]
miR-33 is a highly conserved miRNA family within the intronic sequences of the Srebp genes in organisms ranging from Drosophila to humans.
“We and others provided identification of a highly conserved miRNA family, miR-33, within the intronic sequences of the Srebp genes in organisms ranging from Drosophila to humans (11–14).”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [13]
In mice, there is only one miR-33 gene, conserved with human miR-33a and located within intron 15 of the mouse Srebp-2 gene.
“In mice, however, there is only one miR-33 gene, which is conserved with human miR-33a and located within intron 15 of the mouse Srebp-2 gene.”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [13]
These pathways regulate circulating HDL levels through their roles in HDL biogenesis and cellular cholesterol efflux.
“Importantly, these pathways regulate circulating HDL levels through their roles in HDL biogenesis and cellular cholesterol efflux (12–14).”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [13]
miR-33 participates in the regulation of cholesterol synthesis, fatty acid metabolism, and insulin signaling.
“These microRNAs participate in the regulation of cholesterol synthesis, fatty acid metabolism, and insulin signaling.”
From The Vasculature in Prediabetes (2018) · cites this paper as [143]
miR-33a and miR-33b are co-transcribed and act in conjunction with their host genes, Srebp1 and Srebp2, to regulate cholesterol synthesis.
“They are co-transcribed and act in conjunction with their host genes, Srebp1 and Srebp2, to regulate cholesterol synthesis.”
From The Vasculature in Prediabetes (2018) · cites this paper as [143]
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“…with their host genes, SREBF2 and SREBF1 , which code for transcription factors that regulate cholesterol and fatty acid synthesis/uptake (24–26). miR-33a/b repress the expression of genes involved in pathways that these oppose SREBP-driven functions, including cholesterol efflux ( ABCA1 ,…”
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“The data are supported by three independent studies using different strategies to inhibit endogenous miR-33a, which also increase plasma HDL levels (Marquart et al. 2010, Najafi-Shoushtari et al. 2010, Rayner et al. 2010).”
BackgroundMethodChromatin and beyond: the multitasking roles for SIRT6
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“Reciprocally, the microRNAs miR-33a and miR-33b are generated from the introns of SREBP2 and SREBP1, respectively, and they repress expression of both SREBP itself and SIRT6 [41, 42] (Figure 2).”
BackgroundMicroRNA-mediated regulation of glucose and lipid metabolism
Agbu, P., & Carthew, R. W. (2021) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-021-00354-w · Cited by 368 · see citing works
Mycobacterium tuberculosis induces the miR-33 locus to reprogram autophagy and host lipid metabolism
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“…respectively (mice lack miR-33b) 22, 23, 24, 25 . miR-33a/b repress genes involved in cellular cholesterol export and fatty acid oxidation, including ABCA1, CROT, CPT1, HADHB and PRKAA1, thereby boosting cellular lipid levels and lowering plasma levels of high density lipoproteins 22, 23, 24, 25 .”
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“In humans, SREBP1 and SREBP2 encode miR-33b and miR33a, respectively (15).”
BackgroundHDL-targeted therapies: progress, failures and future
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SREBPs in Lipid Metabolism, Insulin Signaling, and Beyond
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“Feed-forward regulation of SREBPs also leads to the expression of two closely-related microRNAs designated miR-33a and miR-33b that are encoded within introns of the human SREBP-2 and SREBP-1 genes, respectively [24, 25].”
BackgroundAdult-specific functions of animal microRNAs
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Transcriptional control of hepatic lipid metabolism by SREBP and ChREBP
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Control of mitochondrial metabolism and systemic energy homeostasis by microRNAs 378 and 378*
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“MiR-33, encoded by an intron of the sterol regulatory element binding protein gene, has been shown to collaborate with sterol regulatory element binding protein to regulate intracellular cholesterol levels and lipid homeostasis by targeting the adenosine triphosphatebinding cassette transporter A1, a regulator of cell…”
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MicroRNAs in cardiovascular disease: from pathogenesis to prevention and treatment
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“Antisense inhibition of the singular miR-33 species in mice increases total and HDL serum cholesterol concentrations, consistent with increased cellular cholesterol export via the upregulation of ABCA1 in macrophages and hepatocytes (32, 33).”
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“After 7 additional days of eye drops treatment, CNV volume was quantified, and mRNA levels of ABCA1 and ABCG1 were analyzed in mouse tissues.”
InfluentialCell-free 3D scaffold with two-stage delivery of miRNA-26a to regenerate critical-sized bone defects
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Self-citationGenome-wide identification of microRNAs regulating cholesterol and triglyceride homeostasis
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“Another important intronic miRNA is miR-33, which is embedded within the SREBP-2 gene and targets ABCA1 to control cholesterol homeostasis (157, 158).”
BackgroundMicroRNA-148a regulates LDL receptor and ABCA1 expression to control circulating lipoprotein levels
Goedeke, L., Rotllán, N., Canfrán‐Duque, A., Aranda, J. F., Ramírez, C. M., Araldi, E., Lin, C., Anderson, N. N., Wagschal, A., de Cabo, R., et al. (2015) · Nature Medicine · doi:10.1038/nm.3949 · Cited by 270 · see citing works
“…including ours, have demonstrated that miRNAs are a critical component of the cholesterol regulatory circuitry (e.g. the SREBP/miR-33 loci 16,17 and the SREBP-responsive miR-96/182/183 operon 18 ) and have identified a number of miRNAs (miR-122, miR-30c, miR-33a/b, miR-144, miR-223) that…”
Self-citationRole of microRNAs in diabetes and its cardiovascular complications
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“miR-33a and miR-33b have been shown to regulate cholesterol homeostasis through interaction with sterol regulatory elementbinding proteins.(48) Davalos et al.”
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“In macrophages, the SREBP2-coinduced miR-33a targets ABCA1, which impairs reverse cholesterol transport.(5,6) An antigomir against miR-33 decreases atherosclerosis in LDL receptor–null mice, with a concomitant increase in the level of high-density lipoprotein.”
BackgroundATP-Binding Cassette Transporters, Atherosclerosis, and Inflammation
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“Mapping of the sequence reads from small RNA-seq to annotated miRNAs identified 258 expressed miRNAs, including several miRNAs expressed in the mouse liver, such as miR-33, miR-122, miR-103, miR-107, miR-221, and the Let-7 family of miRNAs (Fornari et al., 2008; Frost and Olson, 2011; Jopling et al., 2005; Najafi-Shou…”
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“Likewise, miR-33, which lies in an intron of the sterolresponse-element-binding protein gene (SREBP), regulates cholesterol homeostasis (44).”
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MicroRNA-33 regulates sterol regulatory element-binding protein 1 expression in mice
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microRNA-33 regulates macrophage autophagy in atherosclerosis
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MicroRNA‐33 Deficiency Reduces the Progression of Atherosclerotic Plaque in ApoE <sup>−/−</sup> Mice
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Control of Cholesterol Metabolism and Plasma High-Density Lipoprotein Levels by microRNA-144
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“We and others provided identification of a highly conserved miRNA family, miR-33a/b, within the intronic sequences of the Srebp genes in organisms ranging from Drosophila to humans.(20,21,23) The 3′UTR of Abca1 contains 3 highly conserved binding sites for miR-33a/b, and the expression of ABCA1 mRNA and protein is str…”
BackgroundRegulation of cholesterol homeostasis
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MicroRNAs and Metabolism Crosstalk in Energy Homeostasis
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Roles of microRNA on cancer cell metabolism
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“miR-33 family of microRNAs consists of miR33a and miR-33b, which are encoded within the introns of the SREBF2 and SREBF1 genes, respectively, and are co-expressed in different stimulatory conditions [12,13,32].”
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“inflammation, response to oxidized lipids, oxidative stress, immune function, cholesterol homeostasis, and differentiation.(109,118) –122”
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DNA Methylation of Lipid-Related Genes Affects Blood Lipid Levels
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Mir-33 regulates cell proliferation and cell cycle progression
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“We and others provided the first identification of a highly conserved miRNA family, miR-33, within the intronic sequences of the Srebp genes.(20-22) Two miR-33 genes are present in humans: miR-33b, which is encoded within intron 17 of the Srebp-1 gene on chromosome 17, and miR-33a, which is expressed in intron 16 of t…”
BackgroundMethodNon-coding RNAs: the new central dogma of cancer biology
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“miR-33a, miR-33b Regulate fatty acids, triglyceride, and cholesterol homeostasis, cooperate with the SREBP2 to upregulate intracellular cholesterol levels, have a crucial role in the posttranscriptional repression of ABCA1, which promotes the efflux of free cholesterol from within the cell to ApoA1 and is essential fo…”
BackgroundMicroRNAs and cardiovascular diseases
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MicroRNA-144 Regulates Hepatic ABCA1 and Plasma HDL Following Activation of the Nuclear Receptor FXR
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“…that combines statins and anti-miR-33 oligonucleotides may be useful in hyperlipidemic patients by reversing statin-induced, miR-33-mediated repression of ABCA1, which ultimately would increase plasma HDL (Horie et al, 2010; Marquart et al, 2010; Najafi-Shoushtari et al, 2010; Rayner et al, 2010).”
InfluentialThe Role of the ATP-Binding Cassette A1 (ABCA1) in Human Disease
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“The physiological relevance of miR-33 targeting of ABCA1 was initially demonstrated using miR-33 inhibitors, which caused a two-fold increase of cholesterol efflux from hepatocytes to ApoA-I in vitro [47] and a 30% increase of plasma HDL-C levels in mice [48].”
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“Hence, the expression and activity of miRNAs are interlinked with various cellular processes including development, maintenance of homeostasis, and diseases such as cancer and metabolic disorders [5-7].”
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“Cholesterol/oxysterols might also repress miR33a levels to increase CYP7A1 expression as well as cholesterol efflux transporters.(9) Figure 6 shows a proposed mechanism for the regulation of cholesterol homeostasis by a CYP7A1/SREBP2/miR-33a axis, based on this study, and the well-recognized mechanism for maintaining…”
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- Authors
- Najafi-Shoushtari, S. H., Kristo, F., Li, Y., Shioda, T., Cohen, D. E., Gerszten, R. E., & Näär, A. M.
- Affiliations
- Harvard University (US)
- Massachusetts General Hospital (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Näär, Anders M.
- ORCID
- Venue
- Science
- Published
- 2010-06-18
- Volume
- 328
- Issue
- 5985
- Pages
- 1566-1569
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3840500
- OpenAlex
- W2102901373
- Semantic Scholar
- 8e1f87e5a8c468d11cb938b52c20c8e6954402ce
- Cited by
- 957
- References
- 31
- Citations by year
- 2026: 20 · 2025: 30 · 2024: 24 · 2023: 47 · 2022: 41 · 2021: 56 · 2020: 50 · 2019: 65 · 2018: 66 · 2017: 59 · 2016: 86 · 2015: 88 · 2014: 85 · 2013: 92 · 2012: 73
- FWCI
- 80.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM071449)
- National Institute of Diabetes and Digestive and Kidney Diseases (R21DK084459, R01 DK48873, P30-DK34854, R01DK056626, R01 DK56626, R37DK048873, P30DK034854, R01DK048873)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- miR-33, cholesterol homeostasis, ABCA1, reverse cholesterol transport, HDL synthesis, cholesterol efflux, post-transcriptional regulation, antisense oligonucleotides, locked nucleic acid, cholesterol biosynthesis, cardiometabolic disease
- MeSH terms
- Animals, Cell Line, Cholesterol, Diet, Gene Expression Regulation, Homeostasis, Humans, Introns, Cholesterol, HDL, Liver, Macrophages, Mice, Inbred C57BL, Up-Regulation, Oligonucleotides, Antisense, ATP-Binding Cassette Transporters, 3' Untranslated Regions, RNA Interference, MicroRNAs, Mice, Sterol Regulatory Element Binding Proteins, Sterol Regulatory Element Binding Protein 1, Sterol Regulatory Element Binding Protein 2, ATP Binding Cassette Transporter 1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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