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Statins: mechanism of action and effects
Open accessAbstract
The beneficial effects of statins are the result of their capacity to reduce cholesterol biosyntesis, mainly in the liver, where they are selectively distributed, as well as to the modulation of lipid metabolism, derived from their effect of inhibition upon HMG‐CoA reductase. Statins have antiatherosclerotic effects, that positively correlate with the percent decrease in LDL cholesterol. In addition, they can exert antiatherosclerotic effects independently of their hypolipidemic action. Because the mevalonate metabolism generates a series of isoprenoids vital for different cellular functions, from cholesterol synthesis to the control of cell growth and differentiation, HMG‐CoA reductase inhibition has beneficial pleiotropic effects. Consequently, statins reduce significantly the incidence of coronary events, both in primary and secondary prevention, being the most efficient hypolipidemic compounds that have reduced the rate of mortality in coronary patients. Independent of their hypolipidemic properties, statins interfere with events involved in bone formation and impede tumor cell growth.
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“the Statin class of drugs inhibit 3-hydroxy-3-methylglutaryl (HMG) CoA reductase (HMGCR), the rate-limiting enzyme of de novo cholesterol synthesis5”
From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [5]
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“Statins (3-Hydroxy-3-methylglutaryl CoA reductase inhibitors) inhibit the endogenous synthesis of cholesterol by inhibiting the rate-limiting enzyme of the mevalonate pathway.(14)”
From Effects of coenzyme Q10 supplementation on myopathy in statin-treated patients: a systematic review and meta-analysis (2025) · cites this paper as [14]
In the citing paper
“Statins are competitive inhibitors of HMG-CoA reductase, which catalyses the conversion of HMG-CoA to mevalonate, a rate-limiting step in the isoprenoid biosynthetic pathway, which is involved in the synthesis of cholesterol in humans and ergosterol in fungi [10] .”
From Statins as antifungal agents (2011) · cites this paper as [10]
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Metadata
- Authors
- Stancu, C., & Sima, A.
- Affiliations
- Romanian Academy (RO)
- Corresponding author
- Sima, Anca
- Venue
- Journal of Cellular and Molecular Medicine
- Publisher
- Wiley
- Published
- 2001-10
- Volume
- 5
- Issue
- 4
- Pages
- 378-387
- ISSN
- 1582-1838 (ISSN-L)
- 1582-4934
- PMC
- PMC6740083
- OpenAlex
- W2006572302
- Cited by
- 911
- References
- 42
- Citations by year
- 2026: 35 · 2025: 65 · 2024: 73 · 2023: 81 · 2022: 90 · 2021: 94 · 2020: 96 · 2019: 66 · 2018: 51 · 2017: 48 · 2016: 35 · 2015: 25 · 2014: 34 · 2013: 22 · 2012: 18
- FWCI
- 0.55
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cellular and Molecular Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- statins, HMG-CoA reductase inhibition, cholesterol biosynthesis, lipid metabolism, LDL cholesterol, atherosclerosis, mevalonate metabolism, terpenoids, pleiotropy, coronary events, bone formation, tumor cell proliferation, primary and secondary prevention
- MeSH terms
- Cholesterol Esters, Endothelium, Vascular, Humans, Hypercholesterolemia, Liver, Models, Biological, Muscle, Smooth, Vascular, Molecular Structure, Signal Transduction, Platelet Activation, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Lipid Metabolism
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