Statins: mechanism of action and effects

Stancu, Camelia; Sima, Anca

doi:10.1111/j.1582-4934.2001.tb00172.x

Cited by 912Lipoproteins and Cardiovascular HealthCholesterol and Lipid MetabolismCancer, Lipids, and Metabolism

Statins: mechanism of action and effects

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Stancu, Camelia, Sima, Anca·2001·Journal of Cellular and Molecular Medicine

DOI 10.1111/j.1582-4934.2001.tb00172.xPMC PMC6740083

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Abstract

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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Statins inhibit the endogenous synthesis of cholesterol by inhibiting the rate-limiting enzyme of the mevalonate pathway.
“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]
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 involved in cholesterol synthesis in humans and ergosterol synthesis in fungi.
“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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Stancu C., Niculescu L., Toporan D., Sima A., Ioan A., Simionescu M., Statins produce anti- atherosclerotic effects in coronary heart disease patients, Proceedings of the Romanian Academy, 2001 (in press)

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Authors: Stancu, C., & Sima, A.
Affiliations: Romanian Academy (RO)
Corresponding author: Sima, Anca
ORCID: Stancu, Camelia
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
DOI: 10.1111/j.1582-4934.2001.tb00172.x
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2038 d)
Locations: Journal of Cellular and Molecular Medicine (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Health Sciences › Medicine › Surgery › 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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