Telomere/telomerase system: a new target of statins pleiotropic effect?
Abstract
Statins are well established drugs for primary and secondary prevention of coronary artery disease (CAD). Despite the well-known ability of statins to lower cholesterol, it is now clear that clinical benefits are also substantially higher than expected and several clinical trials, like JUPITER (Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin trial) have indicated that such clinical effects are independent of cholesterol reduction. These cholesterol-independent actions have been named "pleiotropic effects" and include: anti-oxidation and anti-inflammatory effects, modulation of immune activation, stabilization of atherosclerotic plaque, decreased platelet activation, inhibition of cardiac hypertrophy, reduction of cytokine-mediated vascular smooth muscle cell (VSMC) proliferation and improvement of endothelial function. Recently, additional pleiotropic effects of statins on "cellular senescence" have been seen in different cell types, including endothelial progenitor cells (EPC), endothelial cells (EC), VSMC and chondrocytes. At the molecular level, the effect of statins on cellular senescence could be mediated by their interaction with the telomere/telomerase system. Recent evidence suggests that the anti-aging effects of statins are linked to their ability to inhibit telomere shortening by reducing either directly and indirectly oxidative telomeric DNA damage, as well as by a telomere capping proteins dependent mechanism. In this review, we discuss the pleiotropic effects of statins, focusing on the telomere/telomerase system. We will also present our current findings regarding leukocyte telomere length in very old people with myocardial infarction on statin therapy.
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There is preliminary evidence that statins, certain hormones, and caffeine may impact LTL.
“For example, there is preliminary evidence that statins (Olivieri et al., 2012), certain hormones (Lin et al., 2011), and caffeine (Romano et al., 2013) may impact LTL.”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Olivieri et al., 2012
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Self-citation
- Authors
- Olivieri, F., Mazzanti, I., M. Abbatecola, A., Recchioni, R., Marcheselli, F., D. Procopio, A., & Antonicelli, R.
- Affiliations
- Istituti di Ricovero e Cura a Carattere Scientifico (IT)
- Istituto Nazionale di Riposo e Cura per Anziani (IT)
- Venue
- Current Vascular Pharmacology
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2012-03-01
- Volume
- 10
- Issue
- 2
- Pages
- 216-224
- ISSN
- 1570-1611 (ISSN-L)
- OpenAlex
- W2098343552
- Cited by
- 51
- References
- 0
- Citations by year
- 2024: 4 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 5 · 2017: 3 · 2016: 5 · 2015: 11 · 2014: 4 · 2013: 8 · 2012: 1
- FWCI
- 5.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Vascular Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Università Politecnica delle Marche (Università Politecnica delle Marche) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- statins, pleiotropy, cellular senescence, leukocyte telomere length, myocardial infarction, oxidative DNA damage, coronary artery disease, anti-aging effects, endothelial progenitor cells, vascular smooth muscle cells
- MeSH terms
- Aged, Aged, 80 and over, Animals, DNA Damage, Humans, Leukocytes, Telomere, Cellular Senescence, Telomerase, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Telomere Shortening
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