miR‐33 in cardiometabolic diseases: lessons learned from novel animal models and approaches
Open accessAbstract
miRNAs have emerged as critical regulators of nearly all biologic processes and important therapeutic targets for numerous diseases. However, despite the tremendous progress that has been made in this field, many misconceptions remain among much of the broader scientific community about the manner in which miRNAs function. In this review, we focus on miR‐33, one of the most extensively studied miRNAs, as an example, to highlight many of the advances that have been made in the miRNA field and the hurdles that must be cleared to promote the development of miRNA‐based therapies. We discuss how the generation of novel animal models and newly developed experimental techniques helped to elucidate the specialized roles of miR‐33 within different tissues and begin to define the specific mechanisms by which miR‐33 contributes to cardiometabolic diseases including obesity and atherosclerosis. This review will summarize what is known about miR‐33 and highlight common obstacles in the miRNA field and then describe recent advances and approaches that have allowed researchers to provide a more complete picture of the specific functions of this miRNA.
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miR-33b is found primarily in primates and some other mammals and is absent in commonly used rodent models such as mice and rats.
“Notably, miR-33a is highly conserved across a broad range of species, including rodents, whereas miR-33b is only found primarily in primates and some other mammals, being entirely absent in commonly used rodent models, such as mice and rats.”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [8]
The miR-33/SREBP/LXR axis section says miR-33a is conserved across multiple species and rodents lack miR-33b. The paper also discusses miR-33b in humans and non-human primates, but the cited passages do not establish that it is found primarily in primates or specify which other mammals have it. Page numbers are unavailable in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredmiR-33a resides within intron 16 of SREBF2.
“MiR-33a resides within intron 16 of SREBF2, which is primarily involved in the regulation of cholesterol homeostasis genes, such as low-density lipoprotein receptor (LDLR) and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR).”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [8]
miR-33a is highly conserved across a broad range of species, including rodents.
“Notably, miR-33a is highly conserved across a broad range of species, including rodents, whereas miR-33b is only found primarily in primates and some other mammals, being entirely absent in commonly used rodent models, such as mice and rats.”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [8]
miR-33a and miR-33b are embedded within intronic regions of SREBF genes.
“miR-33a and miR-33b are embedded within the intronic regions of SREBF genes.”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [8]
miR-33b is located within intron 17 of SREBF1.
“In contrast, miR-33b is located within intron 17 of SREBF1, which regulates the expression of genes related to fatty acid and triglyceride homeostasis, such as fatty acid synthase (FASN), acetyl-CoA carboxylase α (ACACA) and stearoyl-CoA desaturase 1 (SCD1) 6 - 8) .”
From Critical Role of microRNA-33a/b in Cardiovascular and Metabolic Disease: Molecular Mechanisms and Therapeutic Perspectives (2026) · cites this paper as [8]
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- Authors
- Price, N. L., Goedeke, L., Suárez, Y., & Fernández‐Hernando, C.
- Affiliations
- Yale University (US)
- Venue
- EMBO Molecular Medicine
- Published
- 2021-05-03
- Volume
- 13
- Issue
- 5
- Pages
- e12606-e12606
- ISSN
- 1757-4676 (ISSN-L)
- 1757-4684
- PMC
- PMC8103095
- OpenAlex
- W3158825162
- Cited by
- 36
- References
- 104
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 6 · 2023: 7 · 2022: 7 · 2021: 2
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- EMBO Molecular Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- HHS|NIH|National Heart, Lung, and Blood Institute (R35HL135820, R01HL135012, R01HL105945, K99HL150234)
- HHS|NIH|National Institute of Diabetes and Digestive and Kidney Diseases (1K01DK120794)
- American Heart Association (16EIA27550005)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- miR-33, microRNA, cardiometabolic disease, obesity, atherosclerosis, animal models, miRNA-based therapy, lipid metabolism
- MeSH terms
- Animals, Humans, Models, Animal, MicroRNAs, Atherosclerosis
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