MiR-33 Contributes to the Regulation of 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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Most of the beneficial effects of miR-33 on atherosclerosis have been attributed to its ability to increase circulating levels of HDL-C and/or promote macrophage cholesterol efflux.
“Most of the beneficial effects of miR-33 on atherosclerosis have been attributed to its ability to increase circulating levels of HDL-C and/or promote Mθ cholesterol efflux (Rayner et al., 2011b; 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 Rayner et al., 2010
The paper reports the opposite direction of effect: miR-33 reduces macrophage cholesterol efflux and circulating HDL, while antagonizing miR-33 increases both. It describes these pathways as relevant to atherosclerosis but does not establish beneficial effects of miR-33 on atherosclerosis. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredmiR-33 negatively regulates ABCA1 in both the periphery and the brain.
“Previously, it was shown that miR‐33 negatively regulates ABCA1 in both the periphery and the brain. 15 , 16 , 17 , 18”
From Deletion of miR-33, a regulator of the ABCA1–APOE pathway, ameliorates neuropathological phenotypes in APP/PS1 mice (2024) · cites this paper as [16]
The paper reports that miR-33 represses ABCA1 in macrophages and hepatocytes, supporting regulation in the periphery. It also reports abundant miR-33 expression in mouse brain, but does not show that miR-33 negatively regulates ABCA1 there (searched: brain and brain-related cell types). The indexed copy provides no page numbers for these passages. (LLM, conf=0.87)
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 Rayner et al., 2010
The in vivo mouse passage (indexed under Abstract; Fig. 4D–F, page unavailable) reports that anti-miR-33 increased hepatic ABCA1 protein by 50% and plasma HDL by 25% after six days. It describes lentiviral antagonism, not genetic deletion of miR-33, so the deletion part is not supported by this source. (LLM, conf=0.87)
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 Rayner et al., 2010
The passage labeled Abstract (page not provided) states that hsa-miR-33a is encoded within intron 16 of SREBF2, supporting the miR-33a/SREBP-2 part of the claim. The passages from our copy do not establish that miR-33b is encoded within SREBP-1. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe 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 [12]
The paper’s Abstract identifies ABCA1 as a target of miR-33 in human and mouse cells, and its reporter experiments support direct targeting. Its description of the studied miRNA specifies human miR-33a and its mouse homolog; the copy does not establish the claim for miR-33b or rank ABCA1 as the most well-known target. (LLM, conf=0.84)
Experimental — accuracy not yet measured
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.
“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 [12]
The supplied passages (labeled Abstract; page unavailable) report that anti-miR-33 increased ABCA1 expression in macrophages and hepatocytes, and that mice expressing anti-miR-33 had increased hepatic ABCA1 protein. They do not report results from miR-33a knockout mice; the knockout mice mentioned in the copy are Ldlr−/− and Apoe−/− mice. (LLM, conf=0.87)
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 [16]
In the in vivo mouse experiment (passage [6], labeled Abstract), miR-33 significantly reduced hepatic ABCA1 expression, but the decrease in ABCG1 protein was not statistically significant. The paper also identifies ABCG1 as a miR-33 target only in mice (passage [2]), so it does not establish the unqualified claim that miR-33 targets both genes in vivo. (LLM, conf=0.90)
Experimental — accuracy not yet measuredmiR-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 [14]
The passage on sequence alignment (section labeled Abstract; page unavailable) identifies human and mouse miR-33 within an intron of SREBF2 and says its precursor is highly conserved in mammals. Our copy does not establish a miR-33 family within Srebp genes across organisms ranging from Drosophila to humans. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn 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 [14]
The sequence-alignment passage (indexed under Abstract; page unavailable) identifies mouse mmu-miR-33 as the homolog of human miR-33a and places it in SREBF2. It specifies intron 16, not intron 15, and does not establish that mice have only one miR-33 gene. (LLM, conf=0.90)
Experimental — accuracy not yet measuredTwo 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 [14]
The passage labeled Abstract (page not supplied) identifies human miR-33a within intron 16 of SREBF2. Our copy does not state the chromosome 22 location or identify miR-33b in SREBF1 on chromosome 17, so it supports only part of the attributed sentence. (LLM, conf=0.87)
Experimental — accuracy not yet measuredmiR-33a is cotranscribed with its host gene Srebp-2 and targets genes involved in cholesterol export, including ABCA1, ABCG1, and NPC1.
“We recently showed that miR-33a is cotranscribed with its host gene Srebp-2 like many intronic miRNAs, and it targets genes involved in cholesterol export, including the adenosine triphosphate binding cassette (ABC) transporters ABCA1 and ABCG1 and the endolysosomal transport protein Niemann-Pick C1 (NPC1) (14).”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [14]
The copy identifies hsa-miR-33a within an intron of SREBF2 and describes coincident transcription of SREBF2 and miR-33 (passages 8 and 7, labeled Abstract). It supports ABCA1 and NPC1 as targets, but explicitly limits ABCG1 targeting to mice; the unqualified claim that miR-33a targets ABCG1 omits that species restriction (passages 3–4, labeled Abstract). (LLM, conf=0.87)
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 [14]
The passages labeled Abstract report that miR-33 rises alongside SREBF2 during cholesterol depletion and represses cholesterol export through ABCA1. They also show ABCG1 repression in mouse cells, but state that human ABCG1 lacks miR-33 binding sites. The claim does not qualify its ABCG1 statement by species, despite referring specifically to miR-33a. (LLM, conf=0.88)
Experimental — accuracy not yet measuredInhibition of miR-33a and -b effectively increases HDL in mice.
“Although our previous work in mice supports this contention by showing that inhibition of miR-33a and -b effectively increases HDL (14)”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [14]
The passage on the mouse experiment (indexed under Abstract; page unavailable) reports that anti-miR-33 increased plasma HDL by 25% after six days. The paper identifies the studied mouse miR-33 as the homolog of human miR-33a; our copy does not show that inhibition of miR-33b was tested in mice. (LLM, conf=0.89)
Experimental — accuracy not yet measuredmiR-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 [16]
Changes in Srebp-2 and miR-33a transcription were quite small in the setting of cholesterol depletion.
“Although our previous work established that miR-33a and Srebp-2 are cotranscribed during states of cholesterol depletion (14), the changes in Srebp-2 and miR-33a transcription were quite small in this setting.”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [14]
miR-33a and Srebp-2 are cotranscribed during states of cholesterol depletion.
“Although our previous work established that miR-33a and Srebp-2 are cotranscribed during states of cholesterol depletion (14)”
From miR-33a/b contribute to the regulation of fatty acid metabolism and insulin signaling (2011) · cites this paper as [14]
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 [14]
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“…of miR-33a and miR-33b, are intronic miRNAs encoded within the sterol response binding protein 2 ( SREBP2 ) and SREBP1 genes, respectively 4,5 . miRNA-33a/b provide a critical link between the regulation of cholesterol and fatty acid biosynthesis by SREBPs, and cholesterol ef fl ux,…”
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Yoon, H., Flores, L. F., & Kim, J. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2016.04.020 · Cited by 23 · see citing works
The Role of ATP-Binding Cassette Subfamily A in Colorectal Cancer Progression and Resistance
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Tate, M., Wijeratne, H. R. S., Kim, B., Philtjens, S., You, Y., Lee, D., Gutierrez, D. A., Sharify, D., Wells, M., Perez‐Cardelo, M., et al. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.14243 · Cited by 16 · see citing works
Self-citationBaba, O., Horie, T., Nakao, T., Hakuno, D., Nakashima, Y., Nishi, H., Kuwabara, Y., Nishiga, M., Nishino, T., Ide, Y., et al. (2018) · Molecular and Cellular Biology · doi:10.1128/mcb.00604-17 · Cited by 12 · see citing works
Horie, T., Baba, O., Nishino, T., Yamashita, Y., Tsujisaka, Y., & Ono, K. (2026) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.rv22045 · Cited by 5 · see citing works
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- Authors
- Rayner, K. J., Suárez, Y., Dávalos, A., Parathath, S., Fitzgerald, M. L., Tamehiro, N., Fisher, E. A., Moore, K. J., & Fernández-Hernando, C.
- Affiliations
- Harvard University (US)
- New York University (US)
- Departments of Medicine and Cell Biology, Leon H. Charney Division of Cardiology and the Marc and Ruti Bell Vascular Biology and Disease Program, New York University School of Medicine, New York, NY 10016, USA.
- ORCID
- Venue
- Science
- Published
- 2010-06-18
- Volume
- 328
- Issue
- 5985
- Pages
- 1570-1573
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3114628
- OpenAlex
- W2075728036
- Cited by
- 1,260
- References
- 2
- Citations by year
- 2026: 32 · 2025: 54 · 2024: 49 · 2023: 65 · 2022: 64 · 2021: 67 · 2020: 75 · 2019: 83 · 2018: 85 · 2017: 88 · 2016: 101 · 2015: 107 · 2014: 115 · 2013: 100 · 2012: 93
- FWCI
- 92.91
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG020255, R01 AG02055)
- National Heart, Lung, and Blood Institute (R01HL084312, R01HL074136, P30HL101270)
- 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, SREBP, ABCA1, high-density lipoprotein, microRNA, non-coding RNA, serum cholesterol, cardiovascular disease, cholesterol-lowering therapy
- MeSH terms
- ATP Binding Cassette Transporter, Subfamily G, Member 1, Niemann-Pick C1 Protein, Animals, Carrier Proteins, Cell Line, Cholesterol, Cholesterol, Dietary, Dietary Fats, Gene Expression Regulation, Homeostasis, Humans, Hypercholesterolemia, Introns, Lipoproteins, Lipoproteins, HDL, Liver, Macrophages, Membrane Glycoproteins, Mice, Inbred C57BL, Proteins, Transfection, Apolipoprotein A-I, Macrophages, Peritoneal, ATP-Binding Cassette Transporters, MicroRNAs, Intracellular Signaling Peptides and Proteins, Mice, Sterol Regulatory Element Binding Protein 2, ATP Binding Cassette Transporter 1
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