New compounds able to control hepatic cholesterol metabolism: Is it possible to avoid statin treatment in aged people?
Open accessAbstract
Aging is characterized by the loss of homeostasis that leads to changes in the biochemical composition of tissues, reduced ability to respond adaptively to environmental stimuli, and increased susceptibility and vulnerability to diseases including coronary artery diseases, carotid artery disease and brain vessel disease. Hypercholesterolemia is one of the primary risk factors for these pathologies, whose incidence is highly related to aging. Almost 25% of men and 42% of women older than 65 years have a serum total cholesterol level greater than 240 mg/dL. The mechanisms behind this age-related increase in plasma cholesterol are still incompletely understood, thus, the control of plasma cholesterol content in aged people is more challenging than in adults. In this review the different pharmacological approaches to reduce plasma cholesterol levels, particularly in aged people, will be discussed. In brief, current therapies are mostly based on the prescription of statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) that are pretty effective but that exert several side effects. More attention should be given to potential drug interactions, potential age-related changes in drug pharmacokinetics, adverse effects such as myopathy and competing risks when statins are prescribed to old patients. In combination or in alternative to statin therapy, other agents might be required to reduce low density lipoprotein (LDL) cholesterol levels. Among the available drugs, the most commonly prescribed are those addressed to reduce cholesterol absorption, to modulate lipoprotein lipase activity and bile acid sequestrants: even these pharmacological interventions are not exempt from side effects. The use of antioxidants or organoselenium compounds and the discovery of new proteins able to modulate exclusively LDL receptor recycling such as Proprotein convertase subtilisin kexin 9 and SEC24 offer new pharmacological approaches to selectively reduce the main causes of dyslipidemia.
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These changes suggest that low intracellular cholesterol content, as a consequence of HMGCR activity suppression in RTT fibroblasts, induces the classic feedback mechanism with activation of SREBP2 and the increase of its transcriptional targets such as LDLR and HMGCR.
“These changes suggest that low intracellular cholesterol content, as a consequence of HMGCR activity suppression in RTT fibroblasts, induces the classic feedback mechanism with activation of SREBP2 and the increase of its transcriptional targets such as LDLR (LDL receptor) and HMGCR [23,55,103,104,105,106,107].”
From Loss of Mevalonate/Cholesterol Homeostasis in the Brain: A Focus on Autism Spectrum Disorder and Rett Syndrome (2019) · cites this paper as [107]
The Statins section (page not provided) says that HMGR inhibition lowers intracellular cholesterol and that the reduction stimulates SREBP-mediated LDL receptor synthesis. The Introduction (page not provided) also links SREBP to regulation of HMGR transcription. Neither passage addresses RTT fibroblasts, identifies SREBP2 specifically, or reports an increase in HMGCR expression under the claimed conditions. (LLM, conf=0.86)
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- Authors
- Trapani, L.
- Affiliations
- Roma Tre University (IT)
- Corresponding author
- Trapani, Laura
- Venue
- World Journal of Hepatology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2013
- Volume
- 5
- Issue
- 12
- Pages
- 676
- ISSN
- 1948-5182 (ISSN-L)
- PMC
- PMC3879689
- OpenAlex
- W2020421168
- Cited by
- 14
- References
- 78
- Citations by year
- 2022: 3 · 2021: 1 · 2019: 2 · 2018: 2 · 2017: 1 · 2015: 2 · 2014: 2
- FWCI
- 0.24
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Hepatology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi del Molise (submittedVersion)
- Iris (Roma Tre University) (submittedVersion)
- 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
- hepatic cholesterol metabolism, statins, aging, hypercholesterolemia, LDL cholesterol, statin adverse effects, drug interactions, pharmacokinetics, cholesterol absorption inhibitors, lipoprotein lipase, bile acid sequestrants, antioxidants, organoselenium compounds, PCSK9, Sec24, LDL receptor recycling, dyslipidemia, older adults
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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