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A Century of Cholesterol and Coronaries: From Plaques to Genes to Statins
Open accessAbstract
One-fourth of all deaths in industrialized countries result from coronary heart disease. A century of research has revealed the essential causative agent: cholesterol-carrying low-density lipoprotein (LDL). LDL is controlled by specific receptors (LDLRs) in liver that remove it from blood. Mutations that eliminate LDLRs raise LDL and cause heart attacks in childhood, whereas mutations that raise LDLRs reduce LDL and diminish heart attacks. If we are to eliminate coronary disease, lowering LDL should be the primary goal. Effective means to achieve this goal are currently available. The key questions are: who to treat, when to treat, and how long to treat.
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“The receptors for LDL (LDLR) and transferrin receptor (TFR) are both endocytosed from the cell surface via clathrin-coated vesicles and transported through intracellular recycling pathways (14, 15, 16, 17, 18, 19, 20).”
From The small GTPase RAB10 regulates endosomal recycling of the LDL receptor and transferrin receptor in hepatocytes (2022) · cites this paper as [14]
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“LDLR plays a crucial role in the uptake of LDL-C from the circulation by hepatocytes 1,2,7 .”
From Dietary cholesterol activates a Ral-dependent pathway driving LDLR turnover (2026) · cites this paper as [1]
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“The regulation of LDLR trafficking and turnover is essential for maintaining cholesterol homeostasis and remains a major focus of therapeutic strategies for CVD 1,2,7 .”
From Dietary cholesterol activates a Ral-dependent pathway driving LDLR turnover (2026) · cites this paper as [1]
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“Mutations in LDLR cause familial hypercholesterolemia (FH), characterized by elevated levels of plasma LDL-C and increased risk of coronary heart disease (1).”
From Identification of amino acid residues in the MT-loop of MT1-MMP critical for its ability to cleave low-density lipoprotein receptor (2022) · cites this paper as [1]
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“Elevated LDL-C levels are linked to an increased risk of ASCVD,4,5”
From Sirtuin-1 directly binds and deacetylates hepatic PCSK9 thereby promoting the inhibition of LDL receptor degradation (2025) · cites this paper as [5]
In the citing paper
“Unlike common diseases, the clarity of causation for Mendelian disorders usually simplifies the task of generating models (including human cells and organoids or rodents) to connect genotype to organismal phenotype; these have led to many critical insights into the biology of health and disease in humans98,99.”
From A brief history of human disease genetics (2020) · cites this paper as [98]
In the citing paper
“These data suggest that lifelong lower levels of plasma LDL cholesterol are much more effective than late LDL reductions induced by statins in preventing coronary heart disease (31).”
From Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms (2018) · cites this paper as [31]
In the citing paper
“Hypercholesterolemia is one of the key risk factors in promoting atherosclerosis, which is the underlying cause of approximately 90% of cases of myocardial infarction, 60% of strokes, most cases of chronic heart failure, peripheral arterial disease, and vascular dementia (31).”
From Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms (2018) · cites this paper as [31]
In the citing paper
“An example is the J-shaped association between alcohol consumption and cardiovascular disease; there is now consensus that this apparent protective effect of moderate levels of consumption is artefactual, as discussed above.130”
From Mendelian randomization (2022) · cites this paper as [130]
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“For example, a large-effect genetic variant influencing alcohol consumption that has been of considerable value in MR studies of the effects of alcohol75,130 is only prevalent in East Asian populations.”
From Mendelian randomization (2022) · cites this paper as [130]
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“Statins block cholesterol synthesis by suppressing HMG-CoA reductase91”
From EHBP1 suppresses liver fibrosis in metabolic dysfunction-associated steatohepatitis (2025) · cites this paper as [91]
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Metadata
- Authors
- Goldstein, J. L., & Brown, M. S.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Goldstein, Joseph L.
- Brown, Michael S.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-03
- Volume
- 161
- Issue
- 1
- Pages
- 161-172
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4525717
- OpenAlex
- W2160347316
- Cited by
- 1,233
- References
- 115
- Citations by year
- 2026: 101 · 2025: 134 · 2024: 117 · 2023: 121 · 2022: 136 · 2021: 150 · 2020: 116 · 2019: 105 · 2018: 87 · 2017: 84 · 2016: 61 · 2015: 19
- FWCI
- 16.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Regeneron Pharmaceuticals
- National Heart, Lung, and Blood Institute (HL-20948, P01HL020948)
- 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 › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- cholesterol, coronary artery disease, low-density lipoprotein, LDL receptor, LDLR mutations, familial hypercholesterolemia, statins, lipid-lowering therapy, atherosclerosis
- MeSH terms
- Animals, Cardiovascular Diseases, Cholesterol, Coronary Vessels, Dietary Fats, Humans, Receptors, LDL, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Plaque, Atherosclerotic
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